In most cases, testing for viral infections (e.g., culture) is not performed except in cases where the patient is immunocompromised.

Clinically, distinguishing between seasonal and swine influenza is not necessary, except from an infection control or public health standpoint. Reverse transcriptase-PCR distinguishes between the 2 infections based upon positive reactivity with either the human seasonal influenza panel or the swine influenza panel.

CXR demonstrates findings ranging from focal infiltrates to diffuse infiltrates to lobar consolidation, depending on severity and aetiology of the bacterial infection. Influenza infections can cause interstitial infiltrates, but lobar consolidation is uncommon, unless a secondary bacterial pneumonia is present.FBC may reveal elevated WBC count.Sputum or blood culture may reveal positive Gram stain.

Tests for influenza virus are negative. Reverse transcriptase-PCR is positive for the SARS virus.

Tests for influenza virus are negative. CSF analysis may show increased WBC count, elevated protein, a positive Gram stain (in bacterial meningitis). PCR may be positive for viruses other than influenza in viral meningitis.

MRI: typically, more localised lesions that may be multiple, and with proportionally more vasogenic oedema.Chest-abdominal CT scan, bone scan, and PET scan provide evidence of systemic disease.Histology provides a definitive diagnosis.

MRI demonstrates a thinner capsule toward the ventricle, with restricted diffusion of pus and elevated lactate level; may show multiple lesions.Blood tests suggestive of infection: for example, elevated WBC count, elevated erythrocyte sedimentation rate (ESR), and elevated C-reactive protein (CRP), with sensitivity 90% and specificity 77%. [31]Biopsy or aspiration provides the definite diagnosis, demonstrating pus (inflammatory cells), no tumour cells, and a positive culture of bacterial agent or fungus.

MRI shows multiple lesions in the periventricular white matter; may or may not enhance.CSF shows oligoclonal bands.Histology provides the definitive diagnosis, demonstrating demyelinating lesions, inflammatory cells, and absence of tumour cells, but usually is not necessary.

PET scan is cold.Histology provides definitive diagnosis (no tumour cells and extensive necrosis).

MRI shows typical vasculature distribution and restricted diffusion.

CSF shows leukocytosis, Herpes simplex virus (HSV) antibodies, and/or RBCs.EEG is characteristic with periodic lateralising epileptiform discharges.CT or MRI shows oedematous temporal lobes and haemorrhagic transformation.Brain biopsy is definitive with virus isolation.

CT scan demonstrates calcification in 90% of cases.Cortical location on MRI.Histology provides definitive diagnosis with classic fried egg cytoplasm and chicken wire vasculature.

MRI demonstrates a cortical lesion with distinct margins.CT may show deformity over the calvaria.Histopathology provides definitive diagnosis.

MRI commonly demonstrates medial temporal lobe lesion with cystic components and/or calcifications.Histology is definitive with characteristic cell types: ganglion and glial cells.

Stool guaiac testing may be trace positive.Leukocytosis may be present.CT scan will demonstrate a normal-calibre aorta and possibly diverticula, inflammation of the pericolic fat or other tissues, bowel-wall thickness >4 mm, or a peridiverticular abscess. [54]

Urinalysis positive for blood and may demonstrate crystals and/or evidence of infection.Ultrasound and CT scan will demonstrate a normal-calibre aorta and possibly ureteral or renal stones. [55]

Imaging modalities are often inconclusive, but will demonstrate a normal-calibre aorta.

Anaemia is common.Radiographical imaging (i.e., ultrasound or CT scan) will demonstrate a normal-calibre aorta.Endoscopic evaluation with biopsy shows typical lesions of ulcerative colitis or Crohn's disease. [57]

Leukocytosis and sterile pyuria on urinalysis is common.Imaging with ultrasound or CT scan will demonstrate a normal-calibre aorta with an inflamed appendix or evidence of perforation.

Leukocytosis may be present. Ultrasound will demonstrate a normal calibre aorta and possible reduced or absence of adnexal vascular flow. [58]

Stool is likely to be guaiac positive.Endoscopic evaluation may demonstrate the luminal bleeding source along with mucosal ulcerations, polyps, or tumour.Radiographical imaging with ultrasound or CT scan will demonstrate a normal calibre aorta.

Leukocytosis, haemoconcentration, and systemic acidosis are common with acute splanchnic vessel occlusion. Elevated levels of serum amylase, inorganic phosphorous, creatinine phosphokinase, and alkaline phosphatase may accompany frank bowel infarction.Angiography is diagnostic and potentially therapeutic in the case of vascular occlusion.Ultrasound and CT scan will demonstrate a normal-calibre aorta and will diagnose any splanchnic artery aneurysms. [59]

Blood tests showing low microsomal triglyceride transfer protein (MTTP) and absent or low apolipoprotein B (apo B) aid in differentiation. Colonoscopy and a barium meal and follow-through with X-ray are helpful to identify Crohn's disease.

Blood tests showing low MTTP and absent or low apo B aid in differentiation. Endoscopy with biopsy helps differentiate ulcerative colitis.

Blood tests showing low MTTP and absent or low apo B aid in differentiation.

Blood tests showing low MTTP and absent or low apo B aid in differentiating abetalipoproteinaemia.In child abuse, radiological studies may show multiple healed fractures or suspicious spiral fractures.

In homozygotic hypobetalipoproteinaemia, the patient's parents will have low plasma LDL and low apoprotein B levels. [1]

EEG will be normal.

EEG will be normal. A variety of neuropsychological tests can help with formalising diagnosis.

EEG will be normal, asymmetric, or show focal epileptiform abnormality.

Routine EEG will be normal. It is often necessary to do prolonged video EEG monitoring to completely characterise the event and establish that there is no ictal electrographical abnormality.

Skin biopsy shows variable degrees of epidermal hyperplasia, papillomatosis, and inflammation.Some cases may show features indistinguishable from AN, but there is typically less papillomatosis and more inflammation than seen in AN. [6]As some authors consider AN a type of epidermal nevus, the distinction may be academic in some cases. [4] [6]

Skin biopsy shows filiform downgrowths of epidermis with pigmented rete ridges and occasional pseudohorn cysts, resembling seborrhoeic keratosis.Papillomatosis and hyperkeratosis resembling AN are not seen. [26]

Skin biopsy shows epidermal acanthosis and low papillomatosis (less prominent than AN), and may show basilar pigmentation. [27]There may also be mild telangiectasia and beading of elastic fibres, findings not seen in AN.

Skin biopsy shows epidermal acanthosis with pseudohorn cysts and variable papillomatosis. The lesions are usually more endophytic than AN, and the papillomatosis is more irregular.There is often inflammation and associated squamous differentiation with eddies, findings not seen in AN.

Skin biopsy shows epidermotropism by enlarged, atypical lymphocytes, often with nuclear hyperchromasia and hyperconvolutions.Immunohistochemistry shows an increased CD4:CD8 ratio in most cases. Molecular analysis shows clonal T-cell gene re-arrangement. [28]

Clinical features sufficient to distinguish these entities without further investigation.

On skin biopsy, ichthyosis hystrix may have a pattern of epidermolytic hyperkeratosis or more non-specific findings of hyperkeratosis, hypergranulosis, acanthosis, and papillomatosis. [30]

Pemphigus patients have auto-antibodies that can be detected in the blood or by direct immunofluorescence of skin lesions. [33]

There should be evidence of dermatophyte on scraping for KOH or Periodic Acid-Schiff staining on histology.

Barium swallow and endoscopy will show oesophageal obstruction by the tumour.

Endoscopy will show reflux oesophagitis, with or without a peptic stricture. A hiatus hernia may be present below the stricture.Barium swallow has low sensitivity for oesophagitis but will show up strictures and hiatus hernias. Gastro-oesophageal reflux will be demonstrated.Lower oesophageal pH studies will demonstrate pathological gastro-oesophageal reflux.

Antinuclear antibodies, rheumatoid factor, creatine kinase, and ESR are useful initial screening tests for connective tissue pathology.

Manometry shows high-amplitude oesophageal contractions rather than the aperistalsis usually seen in achalasia.

Oesophageal biopsy shows eosinophilic infiltration (>15 eosinophils per high-power field).

Gastroscopic biopsy of gastro-oesophageal junction and cardia may demonstrate malignancy.Findings at endoscopy, barium swallow, and manometry may be indistinguishable from achalasia.

Microscopic examination of fresh blood showing presence of Trypanosoma cruzi.PCR for precise identification of trypanosome subtype.Giemsa staining of thick and thin blood films detects parasite.

The simplest way to differentiate anti-secretory drug-induced hypochlorhydria and/or hypergastrinaemia as well as nutrient malabsorption is to discontinue the drug and observe return to normal of serum gastrin, iron, cobalamin, and 25-hydroxyvitamin D.

Clinical differentiation usually suffices.

Patch testing will be positive for specific contact allergens.

ANA positive; hypo-complementaemia; anti-Ro antibodies positive; anti-double-stranded DNA antibodies positive.

Positive ANA (speckled and nucleolar immunofluorescence patter); anti-Jo-1 antibody positive.

Clinical differentiation usually suffices.

Elevated 24-hour urinary 5-HIAA levels.

Presence of dense infiltrate of mast cells on tissue biopsy. [9]

Presence of elevated haemoglobin and normal arterial oxygen.

Characteristic granulomatous findings on biopsy of sarcoidal skin lesions, sometimes non-specific.

Clinical differentiation usually suffices.

Clinical differentiation usually suffices.

Clinical differentiation usually suffices.

Clinical differentiation usually suffices.

Skin scraping will demonstrate numerous demodex mites.

Clinical differentiation usually suffices.

Clinical diagnosis usually suffices.

Clinical differentiation usually suffices.Consider laboratory tests such as liver enzymes and lipid panel.

Clinical differentiation usually suffices.Skin biopsy shows increased elastic tissue with thickened, tortuous fibres in the upper and mid-dermis. [27]

Clinical differentiation usually suffices.Pustular lesions that do not respond to typical acne antibiotics may be cultured.

Lesions may be cultured to isolate the gram-negative bacteria if acneiform lesions do not respond to typical antibiotic regimen.

Diascopy reveals yellowish-brown lesions. Skin biopsy reveals caseating epithelioid cell granulomas.

Skin biopsy shows small cysts derived from the infundibulum of the vellus hair.

Clinical differentiation usually suffices.

Skin biopsy shows a grenz zone and mixed inflammatory infiltrate in the upper and mid-dermis, with extravasation of RBCs and haemosiderin deposition.

Clinical differentiation usually suffices.

Skin biopsy shows a dense fibrous stroma with dilated cystic spaces that have small comma-like tails resembling tadpoles.

Skin biopsy shows dermal fibrosis and vascular proliferation and dilation.

CT and MRI imaging findings show a large angle between the tumour and dura not centred over the internal acoustic meatus. Often has a dual tail.Also, imaging displays bone hyperostosis, no internal acoustic meatus enlargement, and no or less extension into the internal acoustic meatus.

MRI imaging shows non-enhancing T1- and T2-weighted images.

CT and MRI imaging results are similar to acoustic neuroma; however, enhancement extends into the geniculate ganglion of the facial nerve and facial canal.

CT and MRI imaging displays a dumbbell-shaped mass over the petrous apex affecting Meckel's cave.The trigeminal nerve enhancement extends proximal to the tumour and does not extend into the internal acoustic meatus.

Degenerative skeletal changes on MRI of the neck.

Mass visualised on neck MRI.

Mass lesion or infarct visualised on brain MRI.

Posterior fossa mass visualised on brain MRI.

Enhancing mass on neck MRI.

Differentiated by clinical examination findings only.

Detection of 36 or more cysteine/arginine/guanine repeats in the Huntington's disease gene.

Differentiated by clinical history and exam findings only. Tics are usually preceeded by premonitory urge followed by release of tension with performance.

Differentiated by clinical examination findings only.

Differentiated by clinical history and exam findings only.

Presence of DYT-1 gene mutation.

Low serum ceruloplasmin, increased urinary copper excretion, mutation in ATP7B gene.

Differentiated by clinical examination findings only.

Insulin-like growth factor 1 normal.Random GH below 0.4 microgram/L (<0.4 nanograms/mL).Oral glucose tolerance test (OGTT) nadir GH below 1 microgram/L (<1 nanogram/mL).Fasting blood sugar and/ or OGTT glucose levels may be markedly elevated.

Skin biopsy shows an intra-epithelial SCC in situ.Atypical (anaplastic) keratinocytes are present throughout the entire epidermis, including follicular infundibulum.There is a thick parakeratotic horny layer and large dyskeratotic cells. Basement membrane is intact. [3] [4] [12] [11] [49] [48]

Skin biopsy shows atypical (anaplastic) keratinocytes throughout entire epidermis, invading dermis.Differentiated tumours have fewer atypical cells and more keratinisation (e.g., horn pearls) than undifferentiated.Anti-cytokeratin 13 antibodies distinguish them from other tumours. [3] [4] [12] [11] [49] [48]

Early lesion skin biopsy shows ill-defined epidermal invaginations into dermis, containing keratinocytes with little nuclear atypia and mitotic figures, and some dyskeratotic cells.Developed lesion biopsy shows a centred crater filled with keratin, surrounded by lip-shaped epidermal extensions. Many horn pearls are seen. [3] [49]

Skin biopsy shows nodular masses of large basaloid cells with large nucleus and little cytoplasm, peripheral palisading that extends into dermis.Cystic spaces present between tumour cells and stroma. [49]

Dermoscopy reveals yellow-white globular structures corresponding with keratin-filled cysts (horny pseudocysts), pseudofollicular openings (yellow-brown crypts), and absent network. [50] [51]

Skin biopsy shows perivascular mononuclear inflammation, interface inflammation with basal keratinocytic vacuolisation, thickening of basement membranes, telangiectasia, epidermal atrophy, and acanthosis. [49] [54] [55]

Skin biopsy shows pseudocarcinomatous epithelial hyperplasia, with a band-like dermal-epidermal junction and perivascular lymphocytic infiltrate, and colloid bodies in the papillary dermis. [56] [57]Very often resembles SCC histologically. [52] [56]

Skin biopsy shows interface lichenoid dermatitis, basal keratinocytic vacuolisation, suprabasilar clefts and vesicles, lymphocytic exocytosis, colloid bodies in lower epidermis and papillary dermis, marked edema, and focal erythrocyte extravasation.Associated with HLA-DR2 and HLA-DR3. Seventy percent are anti-Ro (SS-A)-positive. [49] [58] [61]

Skin biopsy shows acanthosis, focal vacuolisation, and disappearance of granular cells with overlying parakeratosis, oedema, and capillary dilation in elongated papillary dermis.Lymphocytes infiltrate perivascular area. Neutrophils in parakeratotic areas form Munro micro-abscesses, and neutrophils in spinous layer form pustules of Kogoj. [49] [63]

Clinical findings should suffice to distinguish from AKs. Skin biopsy shows characteristic deep invaginations of keratin into the epidermis with central parakeratosis (cornoid lamella). [49]

Skin biopsy shows large keratinocytes with large nuclei arranged in a disorganised pattern. [49]Nuclear dysplasia may be present and mitoses are infrequent. Acanthosis, hypergranulosis, and orthohyperkeratosis may also be present.

Skin biopsy shows elongated, fused rete ridges, with small bud-like extensions. Thin epidermis over the rete ridges. Low epidermis with hyperpigmented basaloid cells and strong DOPA-positive dendritic melanocytes.Dermoscopy: discrete regular network, uniform pigmented background, absent brown globules. [51]

Skin biopsy shows a thick epidermis with papillomatosis, and hyperkeratosis. Elongated rete ridges, focal cell vacuolisation (koilocytotic cells), and parakeratotic cells.PCR HPV-DNA amplification may detect viral antigens including HPV common antigen.In-situ hybridisation may identify viral genomic material. [49]

Skin biopsy reveals characteristic hyperkeratotic epidermis, irregular acanthosis, focal thickening of the granular layer, liquefaction of basement membrane, and band-like lymphocytic infiltrate in the upper dermis. [49]

Histology and culture for actinomycetes are negative.Blood or site cultures identify causative organism.

Histopathology shows malignancy. Histology and culture for actinomycetes are negative.

Histology and culture for actinomycetes are negative.

Sputum smear and culture using KOH preparations or specific stains can confirm diagnosis. Histology and culture for actinomycetes are negative.

Blood cultures may be positive with a bacterial abscess. Histology and culture for actinomycetes are negative.

Histology shows malignant tissue. Histology and culture for actinomycetes are negative.

Histology shows malignant tissue. Histology and culture for actinomycetes are negative.

Colonoscopy shows skip lesions. Biopsy shows characteristic changes. Histology and culture for actinomycetes are negative.

Biopsies show continuous distal disease with characteristic changes and an absence of granulomata. Histology and culture for actinomycetes are negative.

Colonoscopy or sigmoidoscopy may show diverticula. Histology and culture for actinomycetes are negative.

Blood cultures may be positive in pyogenic liver abscess. Histology and culture on aspirated fluid is negative for actinomycetes. Ultrasound demonstrates a variably echoic lesion.

Very high WBC count is common. Sputum Gram stain and culture may reveal a causative pathogen. Histology and culture for actinomycetes are negative.

Sputum cytology may reveal malignant cells. Biopsy shows malignant cells. Histology and culture for actinomycetes are negative.

Modified acid-fast staining of biopsy tissue or other samples allows distinction between Nocardia and Actinomyces.

Culture of vaginal secretions may be positive for a sexually transmitted organism. Endometrial biopsy may show changes of endometritis. Histology and culture for actinomycetes are negative.

Sputum Gram stain and culture may reveal a causative pathogen. Histology and culture for actinomycetes are negative.CXR may typically show focal changes in bacterial pneumonia, with large pleural effusion, cavitating changes indicating an abscess, or multifocal or interstitial changes.

Sputum smear and culture positive for acid-fast bacilli. Tuberculin skin testing is usually positive. Histology and culture for actinomycetes are negative.

Histology and culture of infected tissue are positive for acid-fast bacilli. Tuberculin skin testing is usually positive. Histology and culture for actinomycetes are negative.

Biopsy tissue at laparoscopy shows malignant tissue. Histology and culture for actinomycetes are negative.

Anti-Tropheryma whipplei-positive macrophages, carried out on biopsied tissue, are a diagnostic marker. Polymerase chain reaction testing of duodenal biopsies positive for T whipplei (although carriers may also have positive results).

There is no specific test to confirm the diagnosis.Relative lymphocytosis in WBC differential counts is suggestive.Negative ultrasound or CT findings help exclude other diagnoses.

No specific test unless due to typhoid (Salmonella typhi from stool or blood will confirm the diagnosis).

Technetium pertechnetate scan may show the enhancement of diverticulum if gastric mucosa is present.

Barium enema may demonstrate the intussusception with a coil-spring sign at the point of bowel invagination.

CT scan may show intra-abdominal abscess.Contrast study of the small bowel and colon may show stricture or a series of ulcers and fissures (cobblestone appearance) of mucosa.

Erect CXR and abdominal x-ray may show free air under the diaphragm

Urinalysis positive for blood.Leukocytosis usually absent.Abdominal x-rays or tomogram may show calcified stone.Pyelography and CT scan without oral and IV contrast confirm the diagnosis.

Abdominal ultrasound shows thick wall with peri-cholecystitis collection, and tenderness is present over gallbladder area (Murphy's sign).Hepatobiliary iminodiacetic acid scan will show non-visualisation of gallbladder at >4 hours.

Urine microscopy and culture confirm presence of bacteria.

CT scan may show fluid in the abdomen.Peritoneal fluid shows >500/microlitre count and >25% polymorphonuclear leukocytosis.

Endocervical swab may confirm the pelvic inflammatory disease due to Chlamydia trachomatis. [42]

Clinical diagnosis. No investigation indicated.

HCG hormone level is high in serum and in urine.Ultrasound reveals presence of mass in fallopian tubes.

Ultrasonography shows ovarian cyst and decreased blood flow.

Bilateral alveolar infiltrates can be indistinguishable from those seen in aspiration pneumonitis.

Pulmonary function tests usually show reversible obstructive ventilatory impairment. [39]

Sweat chloride test shows elevated level of chloride. Chest x-ray may reveal bronchiectasis, but CT scan is more sensitive. [40]

Chest x-ray shows peribronchial cuffing and hyperinflation.

Chest x-ray may show lobar consolidation.

Chest x-ray may reveal enlarged pulmonary vessels, cardiomegaly, and pulmonary oedema; the infiltrates improve quickly after diuresis.Brain natriuretic peptide >100 nanograms/L (>100 picograms/mL) makes a diagnosis of heart failure with sensitivity of 90%, specificity of 76%, and predictive accuracy of 83%. [43]

Bilateral alveolar infiltrates can be indistinguishable from those seen in aspiration pneumonitis.Bronchoalveolar lavage cell count reveals >10% neutrophils, and lung biopsy shows diffuse alveolar damage. [36]

Bilateral alveolar infiltrates can be indistinguishable from those seen in aspiration pneumonitis. Bronchoalveolar lavage cell count in organising pneumonia may reveal neutrophilia and sometimes lymphocytosis (but <25% lymphocytes) with eosinophilia (but <25% eosinophils). [36]

Bilateral alveolar infiltrates can be indistinguishable from those seen in aspiration pneumonitis. Bronchoalveolar lavage cell count reveals >25% eosinophils. Eosinophilic pleural effusion is rare. Eosinophilic infiltration and diffuse alveolar damage may be seen on lung biopsy. [44]

Bilateral alveolar infiltrates can be indistinguishable from those of aspiration pneumonitis. Granulomatous and cellular pneumonitis with diffuse alveolar damage may be seen on lung biopsy. Bronchoalveolar lavage cell count shows lymphocytosis (>25%) and sometimes neutrophilia (<10%). [36]

Bilateral alveolar infiltrates can be indistinguishable from those of aspiration pneumonitis. Pulmonary capillaritis, bland haemorrhage, and diffuse alveolar damage seen on lung biopsy.Bronchoalveolar lavage shows progressively bloodier return. Cytology shows RBCs and haemosiderin-laden macrophages.Urinalysis may show proteinuria, haematuria, and red cell casts in cases of pulmonary-renal syndromes. [36]

Bilateral alveolar infiltrates may be indistinguishable from those seen in aspiration pneumonitis. [45]

If the foreign body is radio-opaque, it may appear on a plain x-ray. Otherwise, a CT scan of the chest may suggest an endoluminal obstruction.Fibreoptic bronchoscopy is the definitive test for diagnosis and treatment of a foreign body in the airway.

A video laryngostroboscopic examination may show paradoxical vocal cord movement.The classically observed pattern consists of adduction of the anterior two-thirds of the vocal cords with a posterior diamond-shaped chink. This occurs during inspiration but can be present during the entire respiratory cycle and can also be observed on the flow-volume loop as flattening of the inspiratory limb.

Presence of pulmonary oedema on chest radiographs should guide the clinician to a cardiac cause of symptoms.Brain natriuretic peptide (BNP) may help to exclude cardiac cause if <100 nanograms/L (100 picograms/mL). [28]

No differentiating tests.

Patients with asthma will present with evidence of bronchial hyperreactivity and reversibility on pulmonary function tests more frequently than patients with COPD.

Patients have significantly raised serum levels of serotonin or its metabolites, of which the most important is 5-hydroxyindoleacetic acid.

A low- or intermediate-probability Well's score along with a negative D-dimer assay may rule out this diagnosis.If clinical suspicion warrants, a CT pulmonary angiogram study or V/Q scan can be performed. [29]

Chest radiograph may show pulmonary infiltrates or evidence of bronchiectasis.Skin test reactivity or serum antibodies to Aspergillus are present.Serum IgE is typically >1000 nanograms/mL and there is generally a peripheral blood eosinophilia of >500/mm^3. [30]

If clinical suspicion warrants, a chest radiograph can be performed to assess for a pneumothorax.

Inspiratory and expiratory CXRs may reveal asymmetry of chest expansion, due to the ball-valve mechanism of the foreign body.Bronchoscopy is necessary for diagnosis and retrieval of the foreign body.

Skin prick testing is negative; may provide supportive evidence but is not definitive.

Focal signs of pneumonitis or pneumonia on CXR.Modified barium swallow may confirm diagnosis.

Clinical diagnosis.

Cardiomegaly on CXR.Congenital heart disease and impaired cardiac function are demonstrated on an echocardiogram.

Consolidation on CXR.Raised WBC count, procalcitonin level, and/or CRP in bacterial pneumonia (the last 2 tests are controversial: there are no studies on procalcitonin in asthma, while CRP can also be elevated in asthma). [38]

Pneumothorax is seen on CXR.

Pertussis PCR test for pertussis antigen on nasal swab sample.Absolute lymphocytosis of WBC differential may be present.

Sweat test: sweat chloride ≥60 mmol/L on repeat samples is diagnostic (levels of 40 to 60 mmol/L should be considered indeterminate and suspicious).

Bronchoscopy reveals collapse of the trachea or bronchus during expiration.

In bacterial bronchitis, sputum culture commonly isolates Haemophilus influenzae or Streptococcus pneumoniae. [39]

Exercise testing may reproduce the characteristic symptoms.Spirometry during an episode demonstrates blunting of inspiratory volume loop.

No obstructive pattern on spirometry during a hyperventilation episode.

Exercise testing may help distinguish.

Clinical diagnosis.

ECG shows absence of P waves, presence of characteristic flutter waves that give typical saw tooth appearance in the inferior limb leads, and QRS complexes that are regularly (typically 2:1, 3:1, 4:1) irregular. View image

Classic ECG has shortened PR interval and delta wave on the QRS complex, which may degenerate into AF. View imageAn electrophysiological study with view to curative ablation procedure is suggested for patients with ECG changes suggestive of Wolff-Parkinson-White syndrome who present with AF and rapid ventricular rate.

ECG shows abnormal P waves. In multifocal atrial tachycardia, there are at least 3 different morphologies of P waves. View image

CXR will detect an infiltrate from pneumonia that will not be present in acute bronchitis.

None.

PFT may be useful between bouts of acute bronchitis to diagnose asthma in patients who have residual obstructive findings.

Cultures, polymerase chain reactions (PCR), or direct fluorescent antibody testing for Bordetella pertussis will be positive.

CXR shows pulmonary vascular congestion and may show cardiomegaly in CHF.

Upper GI endoscopy may show oesophageal inflammation or erosions with reflux. pH monitoring also can be helpful for detecting acid in the distal oesophagus.

None.

None; the diagnosis should be made based on history of exposure to agents that can cause a cough.

C-spine x-ray: cancer - single or multiple lesions with bony destruction; osteoarthritis - cervical spondylosis or normal.C-spine MRI: cancer - single or multiple lesions with bony destruction; infection - infected areas of bone (vertebral osteomyelitis) or signs of abscess (epidural abscess).CT scan: signs of meningitis.Bone scan: metastatic neoplastic lesions in the spine.Erythrocyte sedimentation rate, c-reactive protein: elevated in infection, malignancy, or inflammatory arthritis.Full blood count: elevated white blood cell count in infection.Herpes zoster immunohistochemistry: positive in varicella virus.

C-spine x-ray: presence of degenerative joint disease or degenerative disc disease.Cervical MRI: bone destruction, spinal cord or nerve compression, intradural or epidural process.

C-spine x-ray: usually normal.MRI brain and C-spine: usually normal. If chronic, may have cervical muscle asymmetry and nerve root compression.

Punctate staining of the cornea with fluorescein dye; Schirmer's tests with <10 mm; tear break-up time <10 seconds.

Tear break-up time <10 seconds.

No definitive tests; recurrent, bilateral, or persistent cases require blood tests to rule out a systemic inflammatory disease.

No definitive tests.

No definitive tests; recurrent, bilateral, or persistent cases require blood tests to rule out a systemic inflammatory disease.

Marked elevation in intraocular pressure (normal <22 mmHg); thin corneas (pachymetry <520); afferent pupillary defect.

Elevated WBC, and positive blood cultures.

Positive potassium hydroxide (KOH) prep/wet mount and elevated vaginal pH.

Negative urine cultures.

Negative urine culture, positive polymerase chain reaction (PCR) test for Chlamydia.

Negative Prehn's sign: there is no pain relief when the affected hemiscrotum is elevated.Colour duplex ultrasonography has been shown to be useful in differentiating between torsion and inflammatory pathology in cases where the history and clinical findings are equivocal. [15]However, there should be no delay in performing scrotal exploration in cases where testicular torsion is considered a likely differential diagnosis.

Usually diagnosed clinically. Ultrasonography can be used to confirm the diagnosis.

Ultrasonography confirms the presence of a hydrocele containing turbid fluid, with a normal appearance of, and blood flow to, the epididymis and testis.

Usually diagnosed clinically.

Ultrasonography will confirm the presence of a testicular tumour.

Chest imaging may show an enlarged heart and/or pleural effusions. An elevated B-type natriuretic peptide is often present. [129] [130] An echocardiogram may be used to determine cardiac function.

Chest imaging in patients with pneumonia should identify changes consistent with an infiltrative process in the lung parenchyma.

Chest imaging is recommended.

Chest imaging is recommended to exclude a possible pneumothorax in patients with more than mild episodes. [135]

Pulmonary embolus may be diagnosed using D-dimer assay, spiral computed tomography angiogram, or pulmonary angiography in patients with COPD. Test selection should be based on local expertise. Dopplers of the lower extremities may be considered to evaluate for deep vein thrombosis.

An electrocardiogram should be performed for patients who may require hospitalisation for care of an acute exacerbation of COPD, to identify possible cardiac ischaemia and arrhythmias. [46]

An electrocardiogram should be performed for patients who may require hospitalisation for care of an acute exacerbation of COPD or who are experiencing palpitations or dizziness, to identify possible cardiac ischaemia and arrhythmias. [46]

An ABG should be performed for patients who are hypoxaemic or are receiving oxygen therapy who present with an apparent acute exacerbation of COPD.

WCC: elevated.Blood cultures: positive for organism.CXR: consolidation.

CT pulmonary angiography: clot in pulmonary artery.

Reduced peak flow.Spirometry: obstructive pattern, reversibility with beta-agonist inhalers

CXR: reticular infiltrate in the late stages of disease.High-resolution CT scan: ground-glass appearance, reticular infiltrates, honeycombing, and architectural distortion.Spirometry: restrictive pattern.

CXR: diffuse infiltratesPulmonary artery wedge pressure: <18 mmHg

FBC to eliminate leukocytosis.Presence of urinary porphobilinogen (PBG) confirms porphyria.

Delta-aminolevulinic acid (ALA) and coproporphyrin III are markedly increased in urine, and PBG is normal or slightly increased.

Faecal total porphyrins are substantially increased with a marked, isolated increase in faecal coproporphyrin III by high-performance liquid chromatography (HPLC). [13]

Increased plasma porphyrin with a diagnostic fluorescence maximum at neutral pH.Faecal porphyrins are substantially increased with a predominance of coproporphyrin III and protoporphyrin by HPLC. [16] [17]HPLC of urine or faecal sample helps differentiate AIP (predominantly uroporphyrin) from variegate porphyria (predominantly coproporphyrin).

Urine shows RBC casts and/or large amounts of proteinuria.Renal biopsy can distinguish from AIN.

Urine shows sloughed tubular epithelial cells or bland urinary sediment.

Renal blood flow scans or magnetic resonance angiography shows large vessel vascular lesions such as emboli or renal vein thrombosis.

Patients have pyuria with positive urine culture.

HbA1c is elevated.Renal biopsy is diagnostic and shows mesangiolysis, glomerulosclerosis, and Kimmelstiel-Wilson nodules.

Renal biopsy shows focal and segmental sclerosis of the glomeruli.HIV is a known cause, and may be positive.

Renal biopsy shows thickening of basement with subepithelial electron-dense deposits.Chest x-ray or CT scan may show a mass consistent with a lung tumour.Stools may be haem-positive in cases of gastrointestinal malignancy.Hepatitis B and C serologies or rapid plasma reagin (RPR) syphilis test may be positive.

Renal biopsy shows IgA deposits on immunofluorescent examination.

Absence of hepatic encephalopathy. According to the West Haven Criteria, hepatic encephalopathy can be categorised into 4 grades based on severity: [33] [34]Grade 1 hepatic encephalopathy is characterised by sleep reversal, mild lack of awareness, shortened attention span, and impaired computations.Grade 2 is associated with lethargy, poor memory, personality change, and the development of asterixis on physical examination.Grade 3 progresses to somnolence, confusion, disorientation, and physical findings that include hyper-reflexia, nystagmus, clonus, and rigidity.Grade 4 is characterised by stupor and coma.

Normal PT/INR, absence of hepatic encephalopathy (according to the West Haven Criteria as mentioned above). [33] [34] In the presence of coagulopathy associated with cholestatic disorders and vitamin K deficiency, administration of subcutaneous vitamin K would improve PT/INR and may also be considered as a differentiating test.

Normal PT/INR, peripheral blood smear, positive Coombs test, absence of hepatic encephalopathy (according to the West Haven Criteria as mentioned above). [33] [34]

In many cases, the leukemic cells of AML or biphenotypic ALL are poorly differentiated with minimal amount of cytoplasm. These cells are difficult to differentiate from those of ALL. [3] [6]In such a case, bone marrow biopsy, peripheral blood smear, cytochemistry, and immunological marker may be helpful in establishing the diagnosis.The presence of myeloid markers and absence of lymphoid ones favour the diagnosis of AML. Scoring panels enable the diagnosis of biphenotypic leukaemia.

FBC: abnormal lymphocytes; CMV infection and Bordatella pertussis infection may present with significant lymphocytosis. [1] [2]Bone marrow aspiration and biopsy: normal haematopoiesis.Immunophenotyping may show increased numbers of haematogones (normal reactive B-cell progenitors).Epstein-Barr serology: positive.Viral testing: may be positive.Culture of nasopharyngeal secretions: may be positive.

CXR: pulmonary mass.Biopsy: small-cell lung cancer appears histologically as sheets of small round cells with dark nuclei, scant cytoplasm, fine granular nuclear chromatin, and indistinct nucleoli. In addition, immunohistochemical staining reveals positivity for chromogranin, neuron-specific enolase, and synaptophysin.

Biopsy: the Merkel cell exhibits immunocytochemical properties of both epithelial and neuroendocrine cells. Immunoreactivity for intermediate filaments such as the cytokeratins may differentiate Merkel cell from other undifferentiated tumours.

Rhabdomyosarcoma: immunohistochemical staining (IHC) or electron microscopy may provide evidence supporting myogenic differentiation. IHC can detect muscle-specific proteins. [16] [30]

No blast cells in peripheral blood or leucoerythroblastic features. [16] [30]Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.The bone marrow aspiration and biopsy are hypocellular in aplastic anaemia.

No blast cells in peripheral blood or leucoerythroblastic features. [16] [30] Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis. The bone marrow aspiration and biopsy are normocellular in ITP with preservation of all 3 lineages.

Bone marrow biopsy, peripheral blood smear, immunophenotyping, and immunochemistry may be helpful in establishing the diagnosis.Blast cells are positive for deoxynucleotidyl transferase and lack staining for myeloperoxidase; also demonstrate presence of lymphoid markers.

The expression of antigens representing both the myeloid and lymphoid leukaemia in the leukaemic clone suggests biphenotypic leukaemia. Cytogenetics may show Philadelphia chromosome t(9:22).

The distinction between high-risk myelodysplastic syndrome (MDS) and AML is artificial in that it is based on the numbers of blasts present. The estimation of blast counts can be difficult and is subjective. The blood film shows dysplasia in >10% of cells of any lineage and the bone marrow may show up to 19% blasts.Micromegakaryocytes and acquired Pelger-Huet (spectacle eye nucleus) neutrophils are specific for MDS. Associated chromosomal deletions or unbalanced chromosomal abnormalities, particularly of chromosomes 8, 7, and 5, are common. Complex cytogenetic changes may occur.The presence of dysplasia may suggest that AML has evolved from MDS.

The peripheral blood film may be indistinguishable from AML but may have an excess of basophils and eosinophils.The presence of the Philadelphia chromosome t(9:22) (q34;q11) supports a diagnosis of CML but does not exclude Philadelphia chromosome-positive AML.Typically no other karyotypic abnormalities are present.

Blood film shows teardrop RBCs and a leukoerythroblastic film.Bone marrow biopsy shows reticulin fibrosis.

Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.Low percentage of blast cells in peripheral blood (<10%). Precursors are morphologically normal.The bone marrow aspiration and biopsy are hypocellular in aplastic anaemia.Patients should also be evaluated for an underlying paroxysmal nocturnal haemoglobinuria and evidence of intravascular haemolysis (reticulocytosis, elevated serum lactate dehydrogenase, and indirect bilirubin, and decreased haptoglobin). A negative Coombs test is suggestive.

Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.Bone marrow will be hypocellular, and no excess of blasts are present.Megaloblastic erythropoiesis is seen with methotrexate.Bone marrow should be reassessed after holding medication.

Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.Bone marrow shows no excess of blasts but mature haematopoietic cells. Increased macrophage activity and toxic granulation of myeloid cell series may be present suggesting infections; Dohle bodies may also be seen in infections.

Macrocytic anaemia will be present unless there is an associated iron deficiency.Peripheral blood smear shows megaloblastic changes.Serum vitamin B12 levels are low.

May improve with proton pump inhibitors, lifestyle modifications, and H pylori treatment.Normal lipase and amylase.Tonometry may show evidence of reflux.Laboratory evaluation will show normal values of amylase and lipase.Endoscopic evaluation will be diagnostic after visualising erosions, erythema, or ulcers, and allows biopsies to be performed.

Normal lipase. May have elevated amylase (usually less marked than that seen in acute pancreatitis).Plain x-rays show sub-diaphragmatic air.

A swallow study may demonstrate a contracted and abnormal-appearing oesophagus with increased pressures on oesophageal manometry.

Normal lipase and amylase.Acute abdominal series will show ground glass appearance, air-fluid levels, distended bowel loops, absence of distal gas, pneumatosis.An abdomen/pelvic CT scan may be more diagnostic, and will show point of transition and potentially identify aetiology (such as volvulus, hernias, intussusception, masses).

High index of suspicion is necessary to make a rapid diagnosis and improve outcomes. In stable patients, where history and physical examination are equivocal, a CT angiography may be useful as a rapid way to make diagnosis.If too unstable for radiographic evaluation, patients usually go directly to surgery.

Several clinical findings are present more frequently in cholangitis, such as fever (95%), right upper quadrant pain (90%), and jaundice (80%).Normal lipase and amylase.Blood cultures are usually positive, especially during episodes of chills, with Escherichia coli and Klebsiella as the most common micro-organisms isolated from infected bile. [16]

Normal lipase and amylase.Ultrasound will show gallstones, stones within the common bile duct with extra-hepatic and/or intra-hepatic duct dilatation.Chemistry will show biochemical obstruction, with increased levels of total and direct bilirubin, alkaline phosphatase, gamma-GT, and a slight increase in ALT/AST but normal levels of pancreatic enzymes (especially lipase).

Normal lipase and amylase.A right upper quadrant ultrasound will show thickened gallbladder wall, stones with acoustic shadows, biliary sludge, peri-cholecystic fluid, and sonographic Murphy's sign, and allows evaluation of the duct system. Can suggest pancreatic head inflammation. May show mild leukocytosis and a very mild elevation of liver enzymes.A hepatobiliary iminodiacetic acid (HIDA) scan is diagnostic when there is no filling of the gallbladder or with delayed emptying of the radiotracer.

Normal lipase and amylase.Important to obtain serum electrolytes and an FBC.Hypokalaemia and alkalosis may be seen secondary to diarrhoea, vomiting, and dehydration.Stool examination for microscopy, culture, osmolality, ova, parasites, Clostridium difficile toxin, and white blood cells may help in identifying the causative factor.

Normal lipase and amylase.Elevated liver function tests are characteristic. AST/ALT in the range of the 1000 units/L is not rare. Serological titres can make diagnosis of aetiological cause.Radiographic studies not important for its diagnosis.

High index of suspicion of diagnosis is necessary. Angiography and CT scan may be useful in diagnosis as well as lactic acid levels.Normal lipase. May have elevated amylase (usually less marked than that seen in acute pancreatitis).

Elevated cardiac enzymes (creatine kinase or creatine phosphokinase, troponins), ECG changes, and clinical scenario make the diagnosis.Normal lipase and amylase.Cardiac catheterisation, perfusion scans, and echocardiograms are useful during the work-up of cardiac ischaemia.

Direct visualisation of the epiglottis (under controlled circumstances in the operating room, with the immediate capability of intubation should the airway close), or lateral neck x-rays.View image

Imaging studies of the neck may be required to visualise the abscess.

Serum monospot positive for Epstein-Barr virus infection.Atypical lymphocytes in peripheral blood.

Culture recovery of organism.

Imaging studies of the neck demonstrate abscess.

Laboratory testing and imaging are not useful in making the diagnosis of Behcet syndrome, but do play a role in ruling out alternative diagnoses.

Diagnosis is made by clinical presentation and confirmed with skin biopsy.

Coronary artery aneurysms; echocardiography findings are abnormal at any stage in the course of the illness.

Elevated WBC count, atypical lymphocytes.PCR molecular assay is an emerging diagnostic modality.

CT of the neck may be diagnostic and is essential to evaluate the extent of disease.Cytological analysis of fine needle aspirate may establish the diagnosis, although biopsy is usually required.

Diagnosis is based on the history and clinical examination, with exclusion of a systemic aetiology; there are no specific laboratory findings.

Clinical diagnosis with negative urinalysis. Histological examination of the prostate reveals BPH.

Serum PSA elevated and may be extremely high in advanced disease.Histological examination of the prostate reveals prostatic carcinoma.

None. Urine cultures may be positive in acute prostatitis and UTIs.

Urinalysis typically with haematuria, though may be negative (e.g., diluted urine sample).Cystoscopic examination of the bladder demonstrates the presence of a tumour.

Endoscopic examination of the rectum and colon demonstrates the presence of a tumour.The tumour may also be demonstrated on imaging (e.g., barium enema).

Clinical diagnosis. Colour duplex ultrasonography may show enlarged and hyperaemic epididymis.

Imaging studies often show small, irregular, scarred kidneys.

Cervical cultures can identify causative pathogens (e.g., Neisseria gonorrhoeae, Chlamydia trachomatis).Microscopic examination of vaginal discharge demonstrates neutrophils.

No differentiating tests exist.

No differentiating tests exist.

Microscopic analysis shows WBCs in urine obtained after prostate massage or by collection of the terminal portion of a urine sample.

Chest radiography is useful in making the diagnosis.

An acutely elevated serum creatinine is diagnostic of acute kidney injury and indicative of reduced clearance.There are no causes of chronically elevated serum creatinine other than reduced glomerular filtration, except for minor elevations in subjects with increased muscle mass and from certain medicines.Creatinine elevation over time provides a chronological perspective and assists in differentiating acute from chronic kidney disease.Twenty-four-hour urine study for creatinine clearance would demonstrate the level of renal function; the use of 131-I iothalamate is standard for this purpose.

Acutely elevated serum creatinine is diagnostic of acute kidney injury.Minor elevations in creatinine from increased muscle mass may rarely be seen.Twenty-four-hour urine study for creatinine clearance would demonstrate normal renal function.

Discontinuing the medicine should result in normalising of the serum creatinine.Twenty-four-hour urine study for creatinine clearance should demonstrate normal function.

CXR: heart failure is suggested by an enlarged cardiac silhouette, a vascular pedicle width >70 mm, central infiltrates, and Kerley B lines.Brain natriuretic peptide (BNP) levels >500 nanograms/L (>500 picograms/mL) also suggest cardiogenic oedema.Echocardiography and measurement of the pulmonary artery occlusion pressure (PAOP) may be needed if the history and physical and laboratory tests do not rule out cardiogenic pulmonary oedema.

CXR. Severe pneumonia with bilateral infiltrates mimics the radiographic appearance of ALI/ARDS.PaO2. If patients do not have severe hypoxaemia with their pneumonia, they do not have ALI/ARDS.

Meets all the clinical criteria for ALI/ARDS.Best differentiated by history.

A syndrome of hypoxia with infiltrates on CXR.The hallmark is finding sequentially bloodier aliquots of fluid during serial bronchoalveolar lavage.Serological tests to look for autoimmune diseases may help to differentiate from ALI/ARDS. [19]

The hallmark of this disease is increased numbers of eosinophils (upwards of 50%) on bronchoalveolar lavage.

No differentiating investigations.

No differentiating investigations.

Allergen skin-prick testing: wheal and flare reaction after specific allergen is introduced into the skin is 3 mm larger than negative (saline) control.In vitro-specific IgE determination: specific allergen response. [18]

Diagnosis is clinical: there are no differentiating tests.

Diagnosis is clinical: there are no differentiating tests. Radiological tests may exclude features of acute bacterial sinusitis.

Nasal flexible endoscopy can be used to determine the source of infection, either from the adenoids or from the sinuses.

Rigid nasal endoscopy should be performed without anaesthesia and decongestant of the nasal cavity, to evaluate for lack of sensation or bleeding when endoscope is pressed against nasal mucosa.

Urea-to-creatinine ratio is >20:1.Urinalysis: osmolality is normal, sodium levels, ratio of urine to plasma creatinine.Ratio of urine to plasma creatinine levels are high and the urinary sodium concentration is low.

Urinalysis shows proteinuria and microscopic haematuria.

PCR test for smallpox will be positive.PCR test for varicella-zoster virus (VZV) will be negative.Review history of recent smallpox vaccine or other possible exposures. Since natural transmission has been eradicated, new cases would more likely occur through laboratory exposure or as an act of bioterroism. If smallpox is considered a possible diagnosis, immediate consultation should be sought and the patient should be placed in immediate isolation (standard, contact, and airborne). The patient should not be permitted to leave isolation until smallpox has been excluded as a diagnostic possibility. Consultation with local health departments is also highly recommended.

Varicella zoster is a clinical diagnosis based on examination of the rash and history of exposure. Differentiating tests are not usually indicated.

Laboratory tests positive for herpes simplex virus (HSV) 1 or HSV 2.

Patients often have a history of exposure to an agent (medication) associated with the condition.Skin biopsy can be helpful; however, most often the diagnosis is made on clinical presentation. [59]

PCR test for monkeypox will be positive.

Low ACTH due to hypothalamic-pituitary-adrenal axis suppression.

Low ACTH level.Pituitary hormone abnormalities: TSH, prolactin, FSH, LH, GH.CT or MRI brain showing lesion in the pituitary gland or hypothalamus.

Transferrin saturation is increased (50% to 100%) and serum ferritin is substantially elevated (>1.1 to 7.4 micromol/L [90 to 600 mg/dL or 900 to 6000 micrograms/L]).

Elevated T3 and free T4 levels.TSH is suppressed.Radio-iodine scan shows increased uptake in areas of excess thyroid hormone production in toxic nodular goitre and Graves' disease.

Varies with the malignancy type.

Normal or elevated serum cortisol.Low sex steroids, LH, and FSH.

Pathological evaluation reveals non-adenocarcinoma malignant cells.Work-up and treatment strategies will now focus on the specific pathological subtype identified.

Axillary view plain radiograph will show a posterior shoulder dislocation.

Shoulder MRI will show evidence of rotator cuff tear.

Shoulder MRI may show evidence of inflammation in the subacromial space.

MRI may reveal a subluxated long head of the biceps tendon, or demonstrate degeneration within the proximal biceps tendon.

MRI or MR arthrograms demonstrate glenoid labral tears.

Either plain film radiographs or MRI will demonstrate degeneration of the acromioclavicular joint, distal clavicle osteolysis, and cystic formation at the end of the clavicle.Although features suggestive of acromioclavicular joint arthrosis may be present on imaging, clinical examination can be normal.

Plain film radiographs may demonstrate degenerative changes in the cervical spine as well as vertebral body subluxation.MRI of the spine may confirm the radiographic findings and show evidence of cervical nerve root compression.

Hyperkalaemia may be present.Serum ACTH is high.Urine screen for exogenous corticosteroids is negative.Computed tomography of adrenals may show infiltrative or haemorrhagic disease.

Computed tomography or magnetic resonance imaging may show compression.Urine screen for exogenous corticosteroids is negative.

ACTH or other stimulation tests show normal adrenal reserve.If testing shows no evidence of adrenal insufficiency, symptoms are likely due to corticosteroid withdrawal syndrome.

No differentiating tests: differentiated on the basis of history and clinical examination.

No differentiating tests: differentiated on the basis of history and clinical examination.Refraction may reveal high myopia: may not be seen in cases in which a patient has undergone refractive surgery, such as laser-assisted in situ keratomileusis, or cataract surgery with intraocular lens implantation.

No differentiating tests: differentiated on the basis of history and clinical examination.

No differentiating tests: differentiated on the basis of history and clinical examination.Fluorescein angiography may be useful to confirm the presence of angioid streaks.

No differentiating tests: differentiated on the basis of history and clinical examination.

No differentiating tests: differentiated on the basis of history and clinical examination.

Fluorescein angiography, optical coherence tomography, and/or indocyanine green (ICG) angiography can often help to distinguish entities that may mimic AMD.

Fluorescein angiography, optical coherence tomography, and/or ICG angiography can often help to distinguish entities that may mimic AMD.

Fluorescein angiography, optical coherence tomography, and/or ICG angiography can often help to distinguish entities that may mimic AMD.

Serum test positive for hepatitis B surface antigen (HBsAg), hepatitis B virus DNA, or anti-hepatitis B core antigen-IgM antibody.In patients with co-existing ALD and HBV but without cirrhosis, ALT is usually higher than AST.

Serum test positive for anti-hepatitis C virus antibody and hepatitis C virus RNA PCR.Most patients have fluctuating elevation of ALT and AST.In patients with co-existing ALD and HCV but without cirrhosis, ALT is usually higher than AST.

Serum test positive for anti-hepatitis A virus-IgM antibody with marked elevation of serum transaminases.

Ultrasound of gallbladder is the initial test.Nuclear medicine hepatobiliary scan may be helpful in cases where diagnosis is unclear.

Ultrasound of liver with Doppler study can show obstruction, thrombosis, collaterals, and hyperechoic cords replacing normal venous architecture.CT abdomen with contrast might be more precise for this diagnosis.

Severe elevation of AST and ALT with prolonged INR and PT.Serum ammonia may be dramatically elevated.Liver biopsy may be diagnostic but is contra-indicated in coagulopathy, unless done by transjugular approach.

High iron saturation (>45% transferrin saturation) and high ferritin.Positive haemochromatosis gene mutation.Liver biopsy shows excessive iron deposition in hepatocytes.High hepatic iron index.

Increased urinary copper, decreased serum ceruloplasmin.Liver biopsy shows excessive copper deposition by copper measurement.

Liver biopsy may show evidence of hepatocellular injury or cholestatic or mixed pattern of liver injury.

There may be positive or elevated ANA, anti-smooth muscle antibody, or anti-liver, anti-kidney microsomal antibodies.Liver biopsy shows evidence of hepatocellular inflammation with plasma cell infiltrates and interface hepatitis with plasma cell infiltrates.

Clinical diagnosis.

Ultrasound abdomen (also CT or MRI of abdomen) may show dilation of biliary tract.

DSM-IV-TR criteria for non-substance use psychiatric disorders. [1]

DSM-IV-TR criteria for substance use disorders other than alcohol. [1]Urine and/or blood toxicologies indicating presence of other substances.

Qualitative drug screen.

Abnormal LFT, abnormal chemistry panel (from use of medications in chronic liver disease resulting in low sodium or low potassium) or increase in ammonia levels.

Lumbar puncture, blood cultures, and FBC to assess leukocytosis or leukopenia; electrolyte panel for abnormal electrolytes like hyponatraemia. PCR and serology testing can be done based on suspected pathogens.

Lumbar puncture, blood cultures, and FBC to assess leukocytosis or leukopenia; electrolyte panel for abnormal electrolytes like hyponatraemia.

Symptoms commonly occur when blood glucose levels fall below 55 mg/dL and cognitive dysfunction can be seen in normal subjects at levels below 50 mg/dL. [16] [17]

There are no tests that are available in the emergency setting. Routine workup for acute delirium should be done to rule out other causes.CT or MRI may help to exclude other causes and show lesions in midbrain and periventricular region. Diagnostic imaging should not be used to decide treatment for Wernicke's encephalopathy in an emergency setting. [18] [19]

Laboratory tests are not specific to diagnosis of schizophrenia and the accepted criteria for diagnosis come from Diagnostic and statistical manual for mental disorders, fourth edition test revision (DSM-IV-TR).

This is a clinical diagnosis and no laboratory test is used to identify this syndrome.

This is a clinical diagnosis and no laboratory test is used to identify this syndrome.

Toxicological screening is not very helpful in anticholinergic poisoning.

Low levels of thyroid-stimulating hormone (TSH) and elevated T3 and T4 in Graves' disease and elevated T3 in T3 toxicosis. A radioactive iodine scan is helpful in identifying the pattern of uptake in the thyroid gland.

Urine toxicology screen will indicate if the subject has been drinking; however, it may not exclude a diagnosis of head injury. CT scan can be diagnostic.

There are no diagnostic tests for distinguishing these conditions. The distinction is best made in consultation with a psychiatrist.

Skin test for sensitivity to Aspergillus fumigatus: negative.Serum total IgE: in non-allergic asthma, not elevated when patient is not taking systemic corticosteroids (which decrease IgE levels).Serum-specific IgE and serum-specific IgG to A fumigatus: not elevated.

Serum total IgE: not elevated.Serum-specific IgE and IgG to A fumigatus: not elevated.CXR: no new infiltrates from baseline.Skin test for sensitivity to A fumigatus: negative.

CXR: bilateral peripheral or pleural-based infiltrates, described as the photographic negative of pulmonary oedema, are virtually pathognomonic for chronic eosinophilic pneumonia (CEP).Lung biopsy: CEP is characterised by interstitial and alveolar eosinophils and histiocytes. Fibrosis is minimal, and bronchiolitis obliterans organising pneumonia is a commonly associated finding. [33]

CXR: commonly shows transient and patchy opacities without lobar or segmental distribution. [46]Lung biopsy: eosinophilic infiltrates, an eosinophilic vasculitis (especially of the small arteries and veins), interstitial and perivascular necrotising granulomas, and areas of necrosis. [45] [46]

Molecular testing for the FIP1L1/PDGFR-alpha mutation: may be positive for a genetic variant of HES. [48]Bone marrow evaluation: demonstrates increased eosinophils and eosinophil precursors or may confirm a myeloproliferative process. [47]Blood eosinophilia: HES has ≥1.50 x 10^9/L ( ≥1500/microlitre) present on at least 2 occasions in the absence of any other cause. In ABPA the cause is hypersensitivity to the Aspergillus mould, whereas in HES no aetiology is found.

Other than the absence of positive allergy tests, no single, specific differentiating feature exists.

Diagnosis is clinical.

Sinus CT scans are abnormal, by definition, in sufferers of chronic sinusitis.

Diagnosis is usually clinical.

In many cases, the leukemic cells of AML or biphenotypic ALL are poorly differentiated with minimal amount of cytoplasm. These cells are difficult to differentiate from those of ALL. [3] [6]In such a case, bone marrow biopsy, peripheral blood smear, cytochemistry, and immunological marker may be helpful in establishing the diagnosis.The presence of myeloid markers and absence of lymphoid ones favour the diagnosis of AML. Scoring panels enable the diagnosis of biphenotypic leukaemia.

FBC: abnormal lymphocytes; CMV infection and Bordatella pertussis infection may present with significant lymphocytosis. [1] [2]Bone marrow aspiration and biopsy: normal haematopoiesis.Immunophenotyping may show increased numbers of haematogones (normal reactive B-cell progenitors).Epstein-Barr serology: positive.Viral testing: may be positive.Culture of nasopharyngeal secretions: may be positive.

CXR: pulmonary mass.Biopsy: small-cell lung cancer appears histologically as sheets of small round cells with dark nuclei, scant cytoplasm, fine granular nuclear chromatin, and indistinct nucleoli. In addition, immunohistochemical staining reveals positivity for chromogranin, neuron-specific enolase, and synaptophysin.

Biopsy: the Merkel cell exhibits immunocytochemical properties of both epithelial and neuroendocrine cells. Immunoreactivity for intermediate filaments such as the cytokeratins may differentiate Merkel cell from other undifferentiated tumours.

Rhabdomyosarcoma: immunohistochemical staining (IHC) or electron microscopy may provide evidence supporting myogenic differentiation. IHC can detect muscle-specific proteins. [16] [30]

No blast cells in peripheral blood or leucoerythroblastic features. [16] [30]Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.The bone marrow aspiration and biopsy are hypocellular in aplastic anaemia.

No blast cells in peripheral blood or leucoerythroblastic features. [16] [30] Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis. The bone marrow aspiration and biopsy are normocellular in ITP with preservation of all 3 lineages.

In many cases, the leukemic cells of AML or biphenotypic ALL are poorly differentiated with minimal amount of cytoplasm. These cells are difficult to differentiate from those of ALL. [3] [6]In such a case, bone marrow biopsy, peripheral blood smear, cytochemistry, and immunological marker may be helpful in establishing the diagnosis.The presence of myeloid markers and absence of lymphoid ones favour the diagnosis of AML. Scoring panels enable the diagnosis of biphenotypic leukaemia.

FBC: abnormal lymphocytes; CMV infection and Bordatella pertussis infection may present with significant lymphocytosis. [1] [2]Bone marrow aspiration and biopsy: normal haematopoiesis.Immunophenotyping may show increased numbers of haematogones (normal reactive B-cell progenitors).Epstein-Barr serology: positive.Viral testing: may be positive.Culture of nasopharyngeal secretions: may be positive.

CXR: pulmonary mass.Biopsy: small-cell lung cancer appears histologically as sheets of small round cells with dark nuclei, scant cytoplasm, fine granular nuclear chromatin, and indistinct nucleoli. In addition, immunohistochemical staining reveals positivity for chromogranin, neuron-specific enolase, and synaptophysin.

Biopsy: the Merkel cell exhibits immunocytochemical properties of both epithelial and neuroendocrine cells. Immunoreactivity for intermediate filaments such as the cytokeratins may differentiate Merkel cell from other undifferentiated tumours.

Rhabdomyosarcoma: immunohistochemical staining (IHC) or electron microscopy may provide evidence supporting myogenic differentiation. IHC can detect muscle-specific proteins. [16] [30]

No blast cells in peripheral blood or leucoerythroblastic features. [16] [30]Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.The bone marrow aspiration and biopsy are hypocellular in aplastic anaemia.

No blast cells in peripheral blood or leucoerythroblastic features. [16] [30] Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis. The bone marrow aspiration and biopsy are normocellular in ITP with preservation of all 3 lineages.

Scalp biopsy shows melanin casts and trichomalacia. [17]

Scalp biopsy shows hyphae on fungal stain.Fungal culture is positive.

Biopsy shows increased number of telogen follicles.

Rapid plasma reagin (RPR) and fluorescent treponemal antibody absorption test (FTA-ABS) are positive.

Anti-nuclear antibody (ANA) is positive.

Biopsy findings either show a lymphocyte-predominant, neutrophilic-predominant or mixed inflammatory infiltrate (depending on the subtype of scarring alopecia) associated with destruction of hair follicles replaced by scarring.

Pre-and post-bronchodilator spirometry: reversibility of obstruction is moderate in AAT deficiency emphysema, while obstruction is usually fully reversible in asthma.

Obstructive, non-reversible pattern on spirometry, predominantly upper lobe changes on CXR/CT.

Marked dilation of airways on CT.Tests for possible causes may demonstrate the CFTR gene or ciliary dysfunction on biopsy.

Viral hepatitis serology including hepatitis A, B, and C antibodies.

Reduced carbohydrate-deficient transferring (CDT), altered gamma-GT, AST, and ALT.

Iron indices in alpha-thalassaemia will be consistent with iron-deficiency anaemia (low serum iron, high transferrin, low transferrin saturation, and low ferritin). Iron deficiency will also present as a microcytic, hypochromic anaemia; however, it will typically present as an acquired rather than a congenital disorder.RBC count will be high in alpha-thalassaemia and tend to be low or normal in iron-deficiency anaemia.If the diagnosis is in question, a short well-monitored trial of iron repletion will frequently confirm the diagnosis.

Beta-thalassaemia, with impaired beta-globin chain synthesis, will also present as a microcytic, hypochromic anaemia.Hb electrophoresis/HPLC will reveal an increased Hb A2 in most forms of beta-thalassaemia. Beta-globin gene sequencing will detect most but not all underlying molecular defects in beta-thalassaemia. Sequencing will not detect deletional beta-thalassaemias.

Variant haemoglobins, either alone or in combination with other globin diseases, can present as a microcytic, hypochromic anaemia.Many of these will be detected by Hb electrophoresis/HPLC; however, DNA-based globin gene testing may be required to confirm the diagnosis.

Degree of anaemia is typically mild to moderate and normocytic. Anaemia of chronic disease can uncommonly present as a microcytic, hypochromic anaemia.WBC and differential and platelet count may be elevated due to associated infection or inflammation.

Lead poisoning interferes with the enzyme ALA dehydratase and thus with haeme synthesis, and can lead to a microcytic anaemia.Peripheral smear will show basophilic stippling in lead poisoning, and the reticulocyte count will be depressed, in contrast to an elevated reticulocyte count in alpha-thalassaemia. Diagnosis can be confirmed by serum lead levels.

Two populations of red cells may be seen on peripheral smear in SA. Diagnosis is confirmed by bone marrow aspiration and biopsy.

The peripheral smear classically reveals hyper-segmented neutrophils and macrocytosis. Serum B12 level is low, and serum homocysteine and methylmalonic acid levels are elevated.Bone marrow examination, if performed, will reveal hypercellularity and megaloblastic changes. The anaemia will correct with vitamin B12 repletion.

The MCV will be high, and serum homocysteine (but not methylmalonic acid) will be elevated. Serum and RBC folate levels will be low.

Active haemolysis will lead to an elevated LDH, low haptoglobin, indirect bilirubinaemia, and an elevated reticulocyte count. The evaluation must include investigation for both intra-corpuscular (enzyme and membrane defects) and extra-corpuscular (auto-immune mediated haemolytic anaemia, drug-induced haemolysis, or micro-angiopathic causes) aetiologies of haemolysis.

The white cell and platelet counts will frequently be abnormal. The peripheral smear may reveal evidence of the underlying disorder: for example, dysplasia in myelodysplastic syndrome and circulating blasts in acute myeloid or lymphoid leukaemia. An urgent bone marrow aspirate and biopsy are required to confirm the diagnosis.

FBC reveals macro-thrombocytopenia. Due to mutations in the MYH9 gene. [23] [24]

Hearing loss may be sensorineural, conductive, or mixed on formal testing. Renal abnormalities ranging from mild hypoplasia to complete absence may be seen on ultrasound. Mainly due to mutations in the EYA1 and SIX1 genes. [25]

All tests normal except for presence of haematuria of glomerular origin. Thin glomerular basement membrane on electron microscopy and normal immunohistochemical staining for type IV collagens in skin and kidney. COL4A3 and COL4A4 testing is available.

Diagnosis on renal biopsy. Mutations described in INF2, ACTN4, TRPC6, CD2AP, NPHS1, NPHS2, and PLCE1 have been identified, though it is highly genetically heterogeneous.

Mutation screening for mutations in MTTL1, MTTE, and MTTK.

Renal biopsy reveals glomerular deposition of IgA.

Mild memory complaints identified by history or through cognitive screening.Cognitive impairment not severe enough to meet full Diagnostic and Statistical Manual (DAM)-IV criteria for AD supports the diagnosis of MCI.

The Confusion Assessment Method (CAM) screening tool is well validated in distinguishing dementia.Repeated Mini-Mental State Examination (MMSE) or CAM evaluations will show acute fluctuations over time.

Geriatric Depression Scale (long and short form), Hamilton Depression Scale, and Cornell Scale for Depression in Dementia may help to differentiate.Limited or no changes on MRI scanning.

CT or MRI scanning demonstrates areas of past infarction and perivascular ischaemia.

No reliable or valid differentiating test.Brain pathology demonstrates the presence of round, eosinophilic, intraneuronal inclusions called Lewy bodies. Neuropathological findings include neurofibrillary tangles, amyloid plaques, and Lewy neurites.

CT or brain MRI reveals structural atrophy in the frontal and/or temporal lobes.PET or single-photon emission computed tomography (SPECT) scanning shows reduced brain activity in the frontal and temporal lobes.Brain histology may reveal diagnostic findings (such as Pick bodies composed of tau protein, TDP-43 proteinopathy, or FUS proteinopathy).

MRI usually reveals global brain atrophy in patients with PD.

Sporadic form: signal hyperintensity in the caudate nucleus and putamen on diffusion-weighted and fluid-attenuated inversion-recovery MRI often present. Cortical ribboning is also a common feature on these imaging sequences.Pulvinar sign in variant CJD (vCJD) is a common MRI finding.Tonsillar biopsy may be future diagnostic development in vCJD.Characteristic EEG findings are triphasic periodic sharp wave complexes seen on repeated EEG testing.CSF 14-3-3 protein essays are recommended to aid in diagnosis when the clinical suspicion is high.

Complete examination by an ophthalmologist (or optometrist).

Complete examination by an ophthalmologist (or optometrist).

Complete examination by an ophthalmologist (or optometrist), brain and orbital MRI with gadolinium enhancement.

Confirmation with gas chromatography and mass spectroscopy (GC/MS) analysis. Considered the most specific and sensitive test. Will determine the exact compounds and presence of metabolites.A number of compounds (trazodone, ranitidine, ritodrine, chlorpromazine, and promethazine) can give false-positive results for methamfetamine with screening assays such as enzyme-multiplied immunoassay. Mebeverine, doxepin, and its metabolite n-desmethyldoxepin can cause false-positive results if a fluorescence polarisation assay is used. GC/MS does not have this problem.Some drugs are metabolised to amfetamines. Selegiline is metabolised to L-amfetamine and L-methamfetamine and causes a false-positive GC/MS result. Quantitative isomer analysis can distinguish the L from R isomer. Clobenzorex, an anorectic medication from Mexico, is metabolised to D-amfetamine, giving positive screening, GC/MS confirmation, and qualitative isomer analysis.

A negative urine toxicology test differentiates a hypertensive crisis from a drug-abuse symptom.

A negative urine toxicology screen with a positive screen for anticholinergics provides differentiation.A positive response to the cholinesterase inhibitor physostigmine test suggests anticholinergic drug use.

Urine toxicology screen is negative for amfetamines, unless there is concomitant amfetamine use.

Urine toxicology screen is negative for amfetamines, unless there is concomitant amfetamine use.

Characterised by recurrent hypertensive episodes with negative urine toxicology screens.Suggested by marked elevation of unconjugated catecholamines, metanephrines, and vanillylmandelic acid in the 24-hour urine collection test.

Urine toxicology screen is negative for amfetamines, unless there is concomitant amfetamine use.

Urine toxicology screen for amfetamines is negative, unless there is concomitant amfetamine use.

Urine toxicology for amfetamines is negative, unless there is concomitant amfetamine use.

Urine drug screen will differentiate cocaine from amfetamines.

Non-specific laboratory findings, including an elevated WBC count, elevated creatine kinase, and decreased serum bicarbonate concentration. Level for suspected agent causing interaction (if available) may be diagnostic.

GHB and its analogues are not detected on standard drug screens and are rapidly cleared from the urine (75-100 mg/kg may be undetectable in the urine by 12 hours after administration). [44] [45] May require process of elimination of known illicit drug usage.

A period of sedation and behavioural control followed by a more extensive history will allow reassessment after the acute drug effects have worn off.

Carbohydrate-deficient transferrin confirms diagnosis but is not widely available. Serum alcohol >22,440 micromol/L (200 mg/dL) with limited impairment can indicate tolerance to the effects of alcohol but does not diagnose dependence.

Documentation of blood glucose <3.3 mmol/L (60 mg/dL) with accompanying symptoms is crucial to diagnosing clinically significant hypoglycaemia.

Toxicology screening may identify the agent.

Toxicology screening may identify the agent.

Toxicology screening may identify the agent. Other indicators are high gamma-GT on liver function tests and macrocytosis on FBC.

Concentrated urine, haemoconcentration with decreased coagulation, and thrombocytopenia. Elevated WBC count and core body temperature, usually negative drug and alcohol screens.

Subarachnoid haemorrhage identifiable on CT or MRI. LP with blood may indicate cerebral bleeding or traumatic spinal tap. Cerebral angiography confirms the presence of aneurysms.

Urinary catecholamines are elevated, or elevated metanephrines, with normal serum T4.

Elevated levels of T3, T4 and free T4, hyperglycaemia, leukocytosis, and anaemia.

CT head (non-contrast) normal or subtly abnormal, hypodense lesions, and mild mass effect prominent later; CSF for cell count and for Gram stain, bacterial culture diagnostic with identification of organism.

CT head (non-contrast) normal; CSF for Gram stain, bacterial culture diagnostic with identification and recovery of organism.

Bone marrow biopsy, peripheral blood smear, immunophenotyping, and immunochemistry may be helpful in establishing the diagnosis.Blast cells are positive for deoxynucleotidyl transferase and lack staining for myeloperoxidase; also demonstrate presence of lymphoid markers.

The expression of antigens representing both the myeloid and lymphoid leukaemia in the leukaemic clone suggests biphenotypic leukaemia. Cytogenetics may show Philadelphia chromosome t(9:22).

The distinction between high-risk myelodysplastic syndrome (MDS) and AML is artificial in that it is based on the numbers of blasts present. The estimation of blast counts can be difficult and is subjective. The blood film shows dysplasia in >10% of cells of any lineage and the bone marrow may show up to 19% blasts.Micromegakaryocytes and acquired Pelger-Huet (spectacle eye nucleus) neutrophils are specific for MDS. Associated chromosomal deletions or unbalanced chromosomal abnormalities, particularly of chromosomes 8, 7, and 5, are common. Complex cytogenetic changes may occur.The presence of dysplasia may suggest that AML has evolved from MDS.

The peripheral blood film may be indistinguishable from AML but may have an excess of basophils and eosinophils.The presence of the Philadelphia chromosome t(9:22) (q34;q11) supports a diagnosis of CML but does not exclude Philadelphia chromosome-positive AML.Typically no other karyotypic abnormalities are present.

Blood film shows teardrop RBCs and a leukoerythroblastic film.Bone marrow biopsy shows reticulin fibrosis.

Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.Low percentage of blast cells in peripheral blood (<10%). Precursors are morphologically normal.The bone marrow aspiration and biopsy are hypocellular in aplastic anaemia.Patients should also be evaluated for an underlying paroxysmal nocturnal haemoglobinuria and evidence of intravascular haemolysis (reticulocytosis, elevated serum lactate dehydrogenase, and indirect bilirubin, and decreased haptoglobin). A negative Coombs test is suggestive.

Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.Bone marrow will be hypocellular, and no excess of blasts are present.Megaloblastic erythropoiesis is seen with methotrexate.Bone marrow should be reassessed after holding medication.

Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.Bone marrow shows no excess of blasts but mature haematopoietic cells. Increased macrophage activity and toxic granulation of myeloid cell series may be present suggesting infections; Dohle bodies may also be seen in infections.

Macrocytic anaemia will be present unless there is an associated iron deficiency.Peripheral blood smear shows megaloblastic changes.Serum vitamin B12 levels are low.

Presence of specific infectious agent on stool or serological testing.

Stool and antigen testing negative for infectious agents.Typical colonoscopy and biopsy appearance.

Infective organism identified in blood or pus culture.

Aspirate of hepatoma negative for infectious cause.

Key diagnostic test is positive serum antibody for fascioliasis.Eosinophilia.

Positive serum antibody test for echinococcus.Aspiration of cyst should be avoided because of the possibility of anaphylaxis.

Echo meets diagnostic criteria for HCM, such as asymmetric septal hypertrophy.Doppler echo with strain to exclude features of amyloidosis does not show the typical restrictive filling changes seen in amyloidosis.MRI can help distinguish between the 2 syndromes.

Renal biopsy does not stain with Congo red.

Sural nerve biopsy does not stain with Congo red.

Plain x-rays show lytic bone lesions, compression fractures, diffuse osteoporosis.Low Hb.Renal impairment.

MRI cervical spine shows cord compression and multiple spinal root compressions.

Electrodiagnostic studies: multifocal nerve conduction block (with other locations than the usual entrapment sites). High GM1 ganglioside antibody titre (up to 80% of patients). [42]

Electromyography: evidence for myopathy.Clinical examination should not show UMN signs.

Clinical evaluation distinguishes this entity from ALS.

Acetylcholine receptor antibodies present.Tensilon test shows improvement in weakness with acetylcholinesterase inhibitors.Repetitive nerve stimulation may be abnormal in both conditions, but in ALS, the EMG of tongue and facial muscles shows ongoing and chronic denervation.

Electromyography shows only simple fasciculations, without any motor unit potential abnormalities.

Clinical evaluation distinguishes this entity from ALS.

Serial clinical evaluation provides data for diagnosis. EMG excludes the LMN signs.

Serial clinical evaluations used for diagnosis.

Bone marrow biopsy, peripheral blood smear, immunophenotyping, and immunochemistry may be helpful in establishing the diagnosis.Blast cells are positive for deoxynucleotidyl transferase and lack staining for myeloperoxidase; also demonstrate presence of lymphoid markers.

The expression of antigens representing both the myeloid and lymphoid leukaemia in the leukaemic clone suggests biphenotypic leukaemia. Cytogenetics may show Philadelphia chromosome t(9:22).

The distinction between high-risk myelodysplastic syndrome (MDS) and AML is artificial in that it is based on the numbers of blasts present. The estimation of blast counts can be difficult and is subjective. The blood film shows dysplasia in >10% of cells of any lineage and the bone marrow may show up to 19% blasts.Micromegakaryocytes and acquired Pelger-Huet (spectacle eye nucleus) neutrophils are specific for MDS. Associated chromosomal deletions or unbalanced chromosomal abnormalities, particularly of chromosomes 8, 7, and 5, are common. Complex cytogenetic changes may occur.The presence of dysplasia may suggest that AML has evolved from MDS.

The peripheral blood film may be indistinguishable from AML but may have an excess of basophils and eosinophils.The presence of the Philadelphia chromosome t(9:22) (q34;q11) supports a diagnosis of CML but does not exclude Philadelphia chromosome-positive AML.Typically no other karyotypic abnormalities are present.

Blood film shows teardrop RBCs and a leukoerythroblastic film.Bone marrow biopsy shows reticulin fibrosis.

Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.Low percentage of blast cells in peripheral blood (<10%). Precursors are morphologically normal.The bone marrow aspiration and biopsy are hypocellular in aplastic anaemia.Patients should also be evaluated for an underlying paroxysmal nocturnal haemoglobinuria and evidence of intravascular haemolysis (reticulocytosis, elevated serum lactate dehydrogenase, and indirect bilirubin, and decreased haptoglobin). A negative Coombs test is suggestive.

Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.Bone marrow will be hypocellular, and no excess of blasts are present.Megaloblastic erythropoiesis is seen with methotrexate.Bone marrow should be reassessed after holding medication.

Bone marrow aspiration and peripheral blood smear are helpful in differentiating diagnosis.Bone marrow shows no excess of blasts but mature haematopoietic cells. Increased macrophage activity and toxic granulation of myeloid cell series may be present suggesting infections; Dohle bodies may also be seen in infections.

Macrocytic anaemia will be present unless there is an associated iron deficiency.Peripheral blood smear shows megaloblastic changes.Serum vitamin B12 levels are low.

Negative urine test for anabolic steroids.Pelvic ultrasound shows presence of solid, complex, septated, multiloculated mass and high blood flow.CT scan shows peritoneal thickening, enlarged lymph nodes, ascites, omental thickening, or liver metastases.

Negative urine test for anabolic steroids.MRI of abdomen/pelvis typically appears hyper-intense to the liver on T2-weighted images because of their high water content.Appear on CT scan as inhomogeneous masses, often with a central area of low attenuation that represents haemorrhage or necrosis.

Negative urine test for anabolic steroids.Elevated serum 17-hydroxyprogesterone demonstrates deficiency of 21-hydroxylase.

Negative urine test for anabolic steroids.Pelvic ultrasound shows polycystic ovaries.Glucose tolerance test shows insulin resistance.

Negative urine test for anabolic steroids.Gonadotrophin-dependent precocious puberty tends to have both elevated LH and elevated FSH, both of which increase after taking exogenous GnRH.Gonadotrophin-independent precocious puberty patients have low levels of FSH and LH, and these hormones do not rise after GnRH dosing.

Negative urine test for anabolic steroids.

Negative urine test for anabolic steroids.Elevated serum cortisol level.High 24-hour urine cortisol excretion.Positive dexamethasone suppression test (persistently high cortisol after giving dexamethasone).

Negative urine test for anabolic steroids.Gas chromatography/mass spectrometry detection of exogenous drugs may confirm diagnosis.

Negative urine test for anabolic steroids.Gas chromatography/mass spectrometry detection of exogenous drugs may confirm diagnosis.

Negative urine test for anabolic steroids.Decreased haemoglobin level and haematocrit with high reticulocyte count.Increased serum bilirubin concentration.

Negative urine test for anabolic steroids.Elevated indirect bilirubin.Positive hepatitis serology.Toxicology testing may detect drugs or other substances that induce hepatitis (drug-induced hepatitis).

Negative urine test for anabolic steroids.Liver biopsy demonstrates architectural distortion of the liver parenchyma with formation of regenerative nodules.Prolonged prothrombin time and decreased platelet count.

Negative urine test for anabolic steroids.Liver biopsy demonstrates malignancy.

Negative urine test for anabolic steroids.Gallstones occasionally seen on plain x-ray or CT, and reliably identified with ultrasound.

Specific mass spectrometry testing is required to identify these compounds. [38]

Ferritin is typically low (<112 picomol/L (50 nanograms/mL)) in iron deficiency; normal or elevated (>225 picomol/L (100 nanograms/mL)) in ACD. A ferritin level <33 picomol/L (<15 nanograms/mL) strongly suggests iron deficiency. The transferrin saturation is typically <10% in iron deficiency; a value of <5% makes iron deficiency very likely.TIBC is typically elevated in iron deficiency anaemia (>70 micromol/L (400 micrograms/dL)) and reduced (<45 micromol/L (250 micrograms/dL)) in ACD.Soluble transferrin receptor (sTfR) is elevated in iron deficiency, normal in ACD. [7] The ratio of sTfR (mg/L) to log ferritin (micrograms/L) is >2 in iron deficiency.Bone marrow iron is absent in iron deficiency anaemia.

Ferritin less helpful. Lowering the cutoff value from <225 picomol/L (<100 nanograms/mL) to <100 picomol/L (<45 nanograms/mL) increases the likelihood ratio of iron deficiency anaemia from 3.2 to 11.1. A ferritin of <33 picomol/L (<15 nanograms/mL) essentially rules in iron deficiency. [15]It is helpful to know that ferritin is approximately threefold elevated over baseline when inflammation is present. Thus, a ferritin of 100 picomol/L (45 nanograms/mL) in a patient with a recent known value of 33 picomol/L (15 nanograms/mL) would suggest co-existent ACD.

Serum creatinine is typically at least mildly elevated. Rarely, only the creatinine clearance is reduced, as in early diabetic chronic kidney disease.When ACD co-exists with anaemia of renal disease, ferritin (absent in iron deficiency) should be higher than otherwise, and CRP and ESR should be elevated.

Anaemia is typically macrocytic (MCV >100 fL).Serum B12 is low (<200 picograms/mL).

Anaemia is macrocytic (MCV >100 fL).Serum folate low (<2.5 nanograms/mL).RBC folate level <140 nanograms/mL.

MCV is low and MCHC is relatively normal in thalassemia trait, and haemoglobin A2 is increased.Blood smear shows microcytosis and significant poikilocytosis.

Bone marrow examination may show incipient or fully developed aplastic anaemia.Absolute reticulocyte count is typically low for the degree of anaemia in hypoplastic and aplastic anaemia.

MCV normal or mildly increased. FBC may show leukopenia, granulocytopenia, thrombocytopenia, leukocytosis, or thrombocytosis. Peripheral smear may show precursor cells. LDH may be increased.

Biopsy is negative for malignancy in haemorrhoids.

Colonoscopy to identify a mass in the rectum.

No tests can differentiate anal margin cancer from anal cancer.

Evaluation under anaesthesia (EUA) and biopsy showing histopathological evidence of Crohn's disease.

CXR suspicious of sarcoid.EUA and biopsy showing histopathological evidence of sarcoid.

CXR suspicious of TB.EUA and biopsy showing histopathological evidence of TB; culture of tissue from fissure growing Bacterium tuberculosis.

Enzyme-linked immunosorbent assay (ELISA), western blot, RNA test, or DNA polymerase chain reaction (PCR) positive for HIV.

Biopsy of enlarged lymph nodes.

Serum tests positive for syphilis.

EUA and biopsy showing squamous cell carcinoma.

Increased WBC count and increased temperature.CXR with a pulmonary infiltrate is suggestive of underlying pneumonia as source of infection.

Elevated cardiac enzymes (CK and troponin). ECG may show signs of myocardial ischaemia (elevated ST segments or flipped T waves). CXR may show signs of CHF (e.g., pulmonary oedema, changes in the cardiac silhouette).

A drop in haematocrit suggests blood loss.A serum urea/creatinine ratio >20 suggests volume depletion.

There is no differentiating test.

There is no differentiating test.

There is no differentiating test.

Deficiency or underactivity of the C1 esterase inhibitor enzyme.Serum complement C4 and CH50 are low.

Pharyngeal endoscopy by an ENT consultant will not show laryngeal oedema but instead vocal cord adduction.

Imaging and bronchoscopy are used to locate and document the foreign body. If the object inhaled is radio-opaque (e.g., a small coin), a plain radiograph of the chest may show its location.

Serum histamine levels and mast cell tryptase are not elevated.

Urinalysis will show high levels of hydroxy indole acetic acid.

There is no differentiating test.

There is no differentiating test.

There is no differentiating test.

Skin test to suspected seafood is negative. Histamine level in consumed fish elevated.

Clinical diagnosis.

Clinical diagnosis.

Clinical diagnosis.

Clinical diagnosis.

Clinical diagnosis.

Histopathology of a scalp biopsy is characterised by an increased number of catagen and telogen follicles, and the presence of lymphocytic and eosinophilic infiltrates in the peribulbar region.

Hair pull test is usually positive. View imageScalp biopsy does not show miniaturised hair follicles and may appear almost normal except for a variable increase in the proportion of telogen follicles.

Hair pull test is positive only in the active early hair loss phases, but negative in longstanding hair loss. Histopathological evaluation of a scalp biopsy shows a normal-appearing scalp skin.

Hair pull test will be positive.Predominantly anagen hairs present on microscopic examination of biopsy specimen.

Standard diagnostic tests are pelvic ultrasound, although not all women have ovarian cysts, and an androgen profile (total and free testosterone, DHEA-sulphate and sex hormone binding globulin).

Standard screening tests show elevated 24-hour urine free cortisol levels, late-night salivary cortisol, or lack of suppression on overnight dexamethasone test. High-and low-dose dexamethasone suppression may further identify ACTH-dependent or -independent Cushing's syndrome.

Screening test shows elevated serum prolactin levels.

Serum test for TSH shows elevated levels in patients with primary hypothyroidism and low or suppressed levels in patients with primary hyperthyroidism.

Standard screening tests reveal microcytic anaemia, low serum iron and ferritin levels and high iron binding capacity.

CT scan identifies colonic diverticula, pericolic fat stranding, thickened bowel wall, soft tissue swelling, and abscesses in diverticular disease.Once diverticulitis has subsided, colonoscopy may be performed to determine the extent of disease and to aid in differentiation.

Colonoscopy identifies mass lesions, which can then be biopsied.

OGD allows identification and biopsy in most cases.

Proctoscopy demonstrates haemorrhoid lesions.

Colonoscopy identifies polyp lesions.

Colonoscopy identifies patchy inflammation and ulcerations.

Colonoscopy demonstrates continuous erythema, mucosal friability and ulceration, and pseudopolyps in the colon and rectum.

A high WBC count and low serum bicarbonate level aid in identifying ischaemic bowel disease.Colonoscopy identifies petechial haemorrhages with pale, swollen mucosal areas in early ischaemia. Severe ischaemia is associated with grey, cyanotic, or black mucosa.

A technetium Tc-99m pertechnetate scan is the preferred investigation.

On colonoscopy, infectious colitis may display pseudomembranous tissue.Cultures for Clostridium difficile are recommended in addition to conventional pathogens such as salmonella and campylobacter.

Gonioscopy shows an open angle.

Intraocular pressure is normal. Gonioscopy shows an open angle. Optic nerve atrophy (whitening of tissue) in contrast to loss of tissue and cupping.

Intraocular pressure usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal.

Intraocular pressure usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal.

Intraocular pressure usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal.

Intraocular pressure usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal.

Intraocular pressure usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal.

PCR for HSV is positive.

Diagnosis is clinical.

Plain x-rays will not identify a fracture.MRI examination or musculoskeletal ultrasound may show oedema with or without a tear to the lateral ankle ligaments (anterior talofibular ligament and calcaneofibular ligament).

Plain x-rays demonstrate no fracture and an MRI or musculoskeletal ultrasound of the Achilles tendon will demonstrate a tear.

Plain x-rays demonstrate a fracture of the talus.

Plain x-rays demonstrate no fracture but may show tibiofibular widening.

Radiographs of the back may demonstrate degenerative disc disease or the presence of osteophytes.

In DISH there are flowing osteophytes along the anterior margin of the vertebra in the presence of normal vertebral bodies and discs on x-ray. [75]

Hand and foot x-rays may reveal erosive disease.

Pelvic x-rays may demonstrate unilateral sacroiliitis.

Only 30% HLA-B27-positive.May have unilateral sacroiliitis.

Focal spinal abnormalities on x-ray or MRI.Elevated inflammatory markers.

Focal spinal abnormalities on x-ray or MRI.

Radiographs more likely to show vertebral collapse or metastatic deposits.

Presence of homogentisic acid in the blood and urine.

Diagnosis is usually clinical. However, MRI or CT pelvis may be used in difficult-to-examine cases to exclude anal fissure (both investigations are very sensitive and specific for anorectal abscesses).

Diagnosis is clinical.

MRI or CT pelvis may be used in difficult-to-examine cases to exclude pilonidal abscess (both investigations are very sensitive and specific for anorectal abscesses).

MRI or CT pelvis may be used in difficult-to-examine cases to exclude infected epidermoid inclusion cyst (both investigations are very sensitive and specific for anorectal abscesses).

Diagnosis is usually clinical.

Rectal swab for microscopy, Gram stain, and culture usually reveals the causative organism (e.g., Neisseria gonorrhoeae, Chlamydia trachomatis, Herpes simplex, Treponema pallidum).In addition, stool microscopy and culture, serological testing, and tissue biopsy may help confirm diagnosis.

No differentiating test exists.

No differentiating test exists.

TFTs show TSH as normal, high T4 and T3.

A fasting plasma glucose level of ≥126 mg/dL (≥ 6.7 mmol/L) and a plasma glucose of 200 mg/dL (11.1 mmol/L) or increased 2 hours after an oral load of 75 mg glucose,or elevated levels of haemoglobin A1c is diagnostic.

Colonoscopy with biopsy will show inflammatory tissue changes.

Colonoscopy with biopsy will show inflammatory tissue changes.

No differentiating test exists.

FBC may show anaemia. If warranted, biopsy, cytology, and imaging should be carried out.

Distinguished by an HIV test.

MRI reveals fluid around or injury to MCL; ACL appears intact. Subsequent x-rays may reveal calcification along previously injured MCL (Pellegrini-Stieda disease).

MRI reveals disrupted PCL, and an intact ACL.

MRI reveals fluid around or disruption to LCL, with intact ACL.

MRI has excellent sensitivity for meniscal tears, but intra-substance degenerative changes may be misread as acute tears. [63]

Imaging rarely necessary. MRI may show effusion, bone bruising, abnormal signal at posterior capsule, but no frank ligament disruption.

X-rays may reveal dislocation if not yet reduced, or patellar fracture. Lateral subluxation and abnormal patellofemoral relationship often noted. MRI often reveals bone bruising, and may show chondral injury, osteochondral fracture, or loose body. [66]

Wound Gram stain and cultures in bacterial furunculosis should reveal typical pathogens, such as Staphylococcus or Streptococcus.

Blood cultures or tissue cultures will reveal typical pathogens associated with ecthyma gangrenosum, such as Pseudomonas aeruginosa, Staphylococcus, and Candida.

Histological examination of orf reveals epidermal hyperplasia, necrosis, pseudoneoplastic vesicular proliferation, and dermal infiltration with eosinophilic dominance. [53]

Blood or wound cultures would not find B anthracis.

Anthrax cases may be distinguished from influenza by the presence of a widened mediastinum on CXR. Rapid antigen assays and oropharyngeal viral cultures may be useful if positive for influenza.

Blood cultures would not find B anthracis.Rise in titre of Mycoplasma-specific Ig on convalescent serum.Positive molecular diagnosis from nasopharyngeal aspirate, sputum, or throat swabs.

Blood cultures would not find B anthracis.

There are no differentiating tests.

An x-ray shows mediastinal widening much like with a ruptured aortic aneurysm; however, mediastinal changes in anthrax occur early in the infection along with pulmonary oedema.

An x-ray shows mediastinal widening much like with superior vena cava syndrome; however, mediastinal changes in anthrax occur early in the infection along with pulmonary oedema.

A subarachnoid haemorrhage may be differentiated from haemorrhagic meningitis on CT scan, Gram stain, and culture of CSF.

Cultures of blood, peritoneal fluid, or oropharyngeal secretions may yield B anthracis. Standard blood cultures effectively grow B anthracis in 6 to 24 hours. Further confirmatory testing (immunohistochemical staining, gamma phage, PCR assays) must be performed by a reference site of the Laboratory Response Network site, if in the US, or according to local protocols in other countries. [1]

There are no differentiating tests.

Antiphospholipid antibodies may be present but are not a diagnostic criterion for Sneddon's syndrome.

Reduced levels of protein C, free protein S level, and antithrombin III level; prothrombin gene mutation (G-20210-A).

Differentiated from coarctation of the aorta by echocardiogram.Two-dimensional echocardiogram of the aortic valve shows an abnormally narrowed or dysplastic aortic valve.Colour Doppler and pulse Doppler across the aortic valve show turbulent blood flow across the valve and are used to measure the gradient.Patients with aortic coarctation with associated bicuspid aortic valve may also have AS.

Echocardiogram will differentiate the severe narrowing seen in critical coarctation from a frank interruption.

An echocardiogram will differentiate the level of the obstructed or narrowed area in the aorta. Using colour and pulse Doppler, any narrowing in the left ventricular outflow tract can be localised to the valvar, sub-valvar, or supra-valvar area, or across the aortic arch.

Four-extremity BP shows no gradient.Echocardiogram shows normal flow across the aortic arch and normal Doppler of the abdominal aorta.

Renal artery Doppler shows renal artery stenosis.Normal echocardiogram.

A 24-hour urine collection is positive for elevated urine creatinine, metanephrines, and catecholamines.

ECG and troponin T may indicate myocardial infarction or ischaemia.ST segment depression may occur in acute dissection, but ST elevation rare.

ECG typically shows diffuse ST elevation.

CT scan of the chest does not show dissection.

CT scan of the chest does not show dissection.

CT scan of the chest shows pulmonary embolus.

CT scan of the chest shows evidence of tumour.

CXR: pulmonary oedema, enlarged left atrium and left ventricle, and mitral valve calcification.ECG: can present with atrial fibrillation.Echocardiography: for MR it is used to assess left ventricular function.

CXR: pulmonary oedema, enlarged left atrium, and mitral valve calcification.ECG: can present with atrial fibrillation. RVH may also be present.Echocardiography: diagnostic for mitral stenosis.

CXR: LVH, calcified aortic valve.ECG: P-mitrale, LVH with strain pattern, left bundle branch block, or complete AV block.Echocardiography: diagnostic for aortic stenosis.

CXR: may show dilation of main pulmonary artery with right ventricular dilation.ECG: right ventricular hypertrophy is usually present.Echocardiography: diagnostic for pulmonary regurgitation.

Transthoracic Doppler echo will demonstrate no significant pressure gradient (<5 mmHg) across the aortic valve with aortic sclerosis.

In ischaemic heart disease, common ECG findings include Q waves in contiguous leads, and the echocardiogram often shows segments of the myocardium with abnormal systolic thickening or wall motion abnormalities.In AS, Q waves are absent in the ECG; regional wall motion abnormalities are absent on the echocardiogram; and coronary arteries are normal upon cardiac catheterisation.

Typical echocardiography findings include asymmetric hypertrophy with the septal wall most prominently affected. Dynamic obstruction is observed at the subvalvular level, and calcification of the valve is often absent, especially in younger patients. [19]

Diagnosis is based on hx and clinical features.Pathergy test is positive in up to 60% of patients, with highest frequency in those of Middle Eastern origin.May be HLA-B51 genotype, although this association varies with ethnicity.

Incisional biopsy will show malignant disease (most commonly squamous cell carcinoma or lymphoma).

Anaemia is macrocytic (MCV >100 fL); serum folate low (<6 nanomol/L [<2.5 nanogram/mL]); RBC folate level <317 nanomol/L (<140 nanogram/mL).

Ferritin is typically low (<112 picomol/L [<50 nanogram/mL]) in iron deficiency; a ferritin level of <34 picomol/L (<15 nanogram/mL) strongly suggests iron deficiency.

Anaemia is typically macrocytic (MCV >100 fL); serum B12 is low (<148 picomol/L [<200 picogram/mL]).

Diagnosis is based on hx and clinical features.HIV serology will be positive.

Colonoscopy will show mucosal inflammation and discrete deep, superficial ulcers located transversely and longitudinally, creating a cobblestone appearance.Full-thickness bowel biopsies demonstrate transmural involvement with non-caseating granulomas.

Colonoscopy will show rectal involvement, continuous uniform involvement, loss of vascular marking, diffuse erythema, mucosal granularity, fistulas (rarely seen), and normal terminal ileum (or mild 'backwash' ileitis in pancolitis).Bowel biopsies will show mucin depletion, basal plasmacytosis, and diffuse mucosal atrophy.

Diagnosis is suggested by positive immunoglobulin A tissue transglutaminase serology.Duodenal endoscopy will show atrophy and scalloping of mucosal folds, nodularity, and mosaic pattern of mucosa; histology will show presence of intra-epithelial lymphocytes, villous atrophy, and crypt hyperplasia.

Diagnosis is based on hx and clinical features.

Diagnosis is based on hx and clinical features.FBC may show leucopenia.

Diagnosis is based on hx and clinical features.FBC may show leucopenia.

Diagnosis is based on hx and clinical features.FBC may show raised ESR.

Diagnosis is based on hx and clinical features.FBC may show leucocytosis.

Incisional biopsy and histopathology may show characteristic findings of pemphigus: epithelial acantholysis with supra-basal blistering.Direct immunofluorescence will show staining for IgG, C3, or both in a broad linear band on the surface of keratinocytes in the suprabasal epithelium.

Diagnosis is based on history and clinical features.FBC will show lymphocytosis and atypical lymphocytosis.Serology will be positive for EBV-specific antibodies: VCA-IgM, VCA-IgG, EA, EBNA.

Clinical diagnosis.

Clinical diagnosis.

HIV testing positive.

Serum B12 levels below lower limit of normal; macrocytic anaemia; megaloblastic changes in bone marrow cells.

Folate levels below lower limit of normal; macrocytic anaemia; megaloblastic changes in bone marrow cells.

TSH elevated, and free T4 low.

SLE and some other connective tissue disorders can cause pancytopenia through an autoimmune mechanism.Positive ANA and anti-double-stranded DNA can help diagnose SLE.Marrow usually cellular or fibrotic, although rarely may also be hypocellular.

Acid-fast bacilli stain or mycobacterial culture from an involved site can diagnose these infections.Bone marrow is not hypocellular (and may show granulomata in TB).

Bone marrow not hypocellular.Ehrlichiosis IgG titre elevated.

Urine legionella antigen positive.Bone marrow not hypocellular.

Blood cultures positive.Bone marrow not hypocellular.

The following features of the bone marrow examination may suggest MDS: [13]1) prominent dysplasia on marrow or peripheral blood examination (particularly in the myeloid and megakaryocyte lineages; AA can often show some erythroid dysplasia)2) circulating blasts or an increased number of marrow blasts (or CD34+ cells on immunohistochemical staining)3) presence of an increased proportion of ringed sideroblasts in the marrow4) marrow fibrosis5) cytogenetic abnormalities (especially abnormalities of chromosome 5 or 7, trisomy 8, 20q-, trisomy 21 or complex karyotypes), but AA can also be associated with cytogenetic abnormalities.

Peripheral blood smear may show blasts.Bone marrow examination reveals abnormal cell population.

Monoclonal urine Ig spike.Careful bone marrow examination reveals abnormal cell population.

Bone marrow examination reveals abnormal cell population.

Bone marrow examination reveals abnormal cell population, usually clonal.Characteristic Reed-Sternberg cells may be seen on bone marrow biopsy.

Metastatic cells in bone marrow.

CBC shows pancytopenia with neutropenia more pronounced than thrombocytopenia.Peripheral blood smear may show blasts.Bone marrow examination reveals abnormal cell population and may show increased reticulin.

CBC shows pancytopenia but with accompanying monocytopenia.

Bone marrow may show hypocellularity with gelatinous transformation, loss of fat cells, and presence of increased ground substance on haematoxylin and eosin staining.

Lung biopsy does not show asbestos bodies or quantification of mineral content of increased asbestos mineral fibres.

Lung biopsy does not show asbestos bodies or quantification of mineral content of increased asbestos mineral fibres.Immunological markers such as RF and ANA are non-specific and may be present in patient with asbestosis without connective tissue disease. [18]

Presence of IgG antibodies in the blood to the causal antigen, a ground glass appearance on HRCT and granulomas on lung biopsy.

Lung biopsy has pathognomonic giant cells that are unique to the disease.

CXR of silicosis is very different, with small rounded opacities initially beginning in the upper lobes. With progression, these smaller nodules conglomerate into large opacities (progressive massive fibrosis). Unlike asbestos exposure, there are no pleural changes seen.Lung biopsy shows pathognomonic silicotic nodules. Some patients with exposure to asbestos and silica may have radiographical and/or pathological changes of mixed dust.

Imaging shows hilar lymphadenopathy and predominately upper lobe scarring.May be associated with hypercalcaemia.Granulomas on biopsy.

No differentiating investigations.

Diagnosis is confirmed using pulmonary function tests (PFTs). CXR may be normal or may show evidence of underlying infection.

It is not usually necessary to perform stool examinations on patients with viral gastroenteritis. However, a stool sample should be obtained if there is an outbreak, to identify the pathogen as quickly as possible. Stool culture is the most definitive diagnostic test in identification of viral pathogens, but this is not practical in most cases. Latex agglutination tests, polymerase chain reaction (PCR), microscopy, enzyme immunoassay (EIA), or serology allows rapid detection, but these are usually not necessary.

Patients with amoebiasis may have stool ova and parasites positive for characteristic trophozoites or cysts, or a positive serological test for Entamoeba histolytica.

Stool or blood culture may grow Salmonella.

Patients with strongyloidiasis may have larvae in stool or sputum, or a positive serology test for S. stercoralis.

Raised serum amylase and lipase are key to diagnosis.

Ultrasound of RUQ may show pericholecystic fluid, distended gallbladder, thickened gallbladder wall, or gallstones.

Diagnosis is usually clinical. However, an FBC could show mild leukocytosis. Further investigations, such as abdominal ultrasound or CT, are indicated in atypical presentations.

Stool studies may demonstrate hookworm eggs.Eggs are not noted in stool studies in patients who are host to the dog or cat hookworm.Patients with hookworm infection may demonstrate hypochromic microcytic anaemia on FBC.

Stool studies reveal characteristic eggs. Anoscopy may also demonstrate worms on visualisation of the rectum.

Transabdominal ultrasound: pericholecystic fluid and gallbladder wall thickening.Abnormal hepatic imido-diacetic acid (HIDA) scan.

LFTs typically normal.

Amylase: greater elevation when compared with cholangitis.Lipase: raised levels are more specific to the pancreas than amylase levels.CT scan: often shows stranding around the pancreas.

Ultrasound, CT, or MRI will typically identify the abscess.

Urinalysis: pyuria, positive nitrites.CT scan may show perinephric stranding.

CT scan of the abdomen: fat stranding around the appendix, thickening of the appendix, periappendiceal fluid.

CT scan of the abdomen usually images the lower lung lobes and will show a consolidation.

Fibrin degradation products: raised.Lactate dehydrogenase: raised (marker of haemolysis).Urinalysis: proteinuria.

If the person meets the autistic disorder criteria, then they should be assigned that diagnosis, as per the hierarchy rule. This means that autistic disorder takes priority over AS, such that if an individual meets the criteria for both (which is possible), then they should be given the diagnosis of autistic disorder, not AS.However, specific communication impairments are also needed for a diagnosis.

PDD-NOS is easily differentiated from AS on the basis of whether the threshold number of diagnostic items is reached. Diagnosis is made clinically, and is essentially reserved for individuals who have the social impairments seen in other ASDs, but do not meet all the essential criteria for any of the specific disorders.

Schizoid personality disorder is differentiated from AS during the clinical interview on the basis of, 1) social aloofness, 2) later onset, and 3) lack of ritualistic or repetitive patterns of behaviour.

Social anxiety should be suspected in any person who describes a clear onset of somatic anxiety symptoms in social situations, but whose social and behavioural development is otherwise inconsistent with AS.

Interestingly, a similar pattern of cognitive strengths and vulnerabilities has also been recorded among children with AS. The nosological validity of NLD compared with AS has not been established, and so the use of this term diagnostically is not encouraged.This is a diagnosis based on the individual's pattern of verbal and performance IQ scores. If diagnosis for AS is met, this should be made as the preferred diagnosis.

This is a diagnosis based on the individual's pattern of communicative strengths and vulnerabilities. However, with its diagnostic validity being poorly established, if criteria for a diagnosis of AS are met, this should be made as the preferred diagnosis.

A diagnostic interview will differentiate between ADHD and AS.

A diagnostic interview will differentiate between bipolar disorder and AS.

Meets the DSM-IV-TR (or ICD-10 criteria) diagnostic criteria for OCD.

Culture and histopathology of tissue and specimens. [81] While Zygomycetes appear as broad, non-septate hyphae with branches occurring at right angles, Aspergillus appears as narrower, septate hyphae with frequent acute-angle branching. Often, these 2 entities may be difficult to distinguish. Blood cultures are negative in zygomycosis as with aspergillosis.No serological test is available.Radiological appearance is similar to that of aspergillosis.

Blood cultures are frequently positive. [82]Tissue cultures help to distinguish the pathogens; histologically Fusarium resembles Aspergillus.No serological test is available.Radiological features and host characteristics are similar to those of aspergillosis. [82]

Tissue cultures help to distinguish the pathogens; histologically, Scedosporium resemble Aspergillus.No serological test is available.Radiological features and host characteristics are similar to those of aspergillosis. [82]

As the host characteristics and clinical/radiological features are similar, culture/histology of the lesion (skin, lung nodule, brain mass/abscess) is required for diagnosis. [83] Histologically, Nocardia appears as gram-positive, branching, slender, filamentous organisms (acid-fast smear positive). Not infrequently, respiratory secretions or aspirate from abscess may reveal the organism.Rarely, standard blood cultures are positive with prolonged incubation.

Nodules and cavities on CXR or chest CT scan may be seen.Respiratory secretions (sputum, bronchoalveolar lavage (BAL) fluid) are helpful for diagnosis.Occasionally, biopsy of involved lungs for mycobacterial stain and culture is needed.

Gram stain and bacterial cultures if available, or BAL fluid, are useful for diagnosis.Blood cultures may be positive.CT-guided needle aspiration of the pulmonary lesion may be required for diagnosis.

Gram stain and bacterial cultures if available, or BAL fluid, are useful for diagnosis.Blood cultures may be positive.CT-guided needle aspiration of the pulmonary lesion may be required.

Gram stain and bacterial cultures if available, or BAL fluid, are useful for diagnosis.Blood cultures may be positive.CT-guided needle aspiration of the pulmonary lesion may be required.

CXR or chest CT scan of chest typically shows wedge-shaped, peripheral pulmonary emboli/infarcts, at times mimicking findings of aspergillosis; however, multiple nodules, 'halo sign', and cavities are generally not seen.

Comparison of serially obtained CXR/CT scans of chest is extremely helpful to distinguish pre-existing malignancy from recent pulmonary aspergillosis.Biopsy of the lesion is required for definitive diagnosis.Anecdotal data suggest that PET-CT scan may be useful to distinguish malignancy from an opportunistic process.

CXR is usually undertaken early in the work-up of chest symptoms. Skin testing, serology testing, and high-resolution CT of the chest are usually performed.

Sputum Gram stain shows no WBCs.

Lack of leukocytosis, or other markers of active infection. CXR usually shows changes in posterior dependent aspects.

CXR typically shows symmetric distribution of opacities, although may not be evident early on. Evaluation of left ventricular dysfunction by BNP and echo are helpful.Leukocytosis usually not present.

CT can occasionally demonstrate low attenuation areas (-30HU).

Common organisms detected on sputum culture are Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Moraxella catarrhalis, Klebsiella pneumoniae, and other gram-negative bacilli.Atypical organisms may be detected with appropriate testing (e.g., serology or antigen tests).

Sputum culture showing growth of gram-negative rods or Staphylococcus aureus is more likely.

Sweat chloride testing: level of sweat chloride >67 mEq/L.Consider repeat testing.

Anterior rhinoscopy or nasal endoscopy may show inflammation, purulent discharge, oedema, or frank polyps.CT may show opacification of involved sinuses, mucosal thickening, air-fluid levels, or anatomic abnormalities.

The sensitivity of plain x-rays is 62%, using microlaryngoscopy and bronchoscopy as the reference standards.In addition to CXR, barium oesophagography is useful for evaluating associated disease processes, such as tracheo-oesophageal fistula and reflux disease.

CT chest with contrast: double aortic arch, abnormal take-off of the innominate artery, anomaly of left pulmonary artery, right aortic arch, aberrant right subclavian, enlarged pulmonary veins. [41]

CXR, CT chest, or bronchoscopy shows the foreign body.

Direct visualisation of the vocal cords with rhinolaryngoscopy during a spell. Inspiratory flow volume loop is helpful when abnormal (flattened).

Testing for the alpha-1 antitrypsin phenotype.

PFTs with residual volume (RV), total lung capacity (TLC), and a flow volume loop with bronchodilator showing an obstructive pattern with an increase in TLC and RV and a reduction in forced expiratory flow at one second (FEV1), FEV1/forced vital capacity (FVC) ratio with no response to bronchodilator.CXR showing hyper-inflation of the lungs.

High-resolution CT chest: dilated airways, bronchial wall thickening.Can occasionally be seen on CXR.

Pulmonary angiogram is the preferred test, but carries risks.An acceptable alternate test is CT angiogram of the lung, which, if not available, can be replaced with the less sensitive V/Q scan.

CXR may show increased alveolar markings, fluid in fissures, and pleural effusions.Echocardiogram: reduced left ventricular ejection fraction.

Serum IgG level <5g/L (500 mg/dL).

Non-atopic result on skin prick testing may provide supportive evidence, but this is not definitive. Causes include respiratory syncytial virus and parainfluenza viruses. [15]

None reliable.Data shows that the new classification of recurrent wheeze may fluctuate during the preschool years. [47] [48]

Inspiratory and expiratory chest radiographs may reveal asymmetry of chest expansion due to the 'ball-valve' mechanism of the foreign body. Chronic changes include collapse and consolidation distal to the obstruction.Bronchoscopy is necessary for confirmation of the diagnosis and retrieval of the foreign body.

Focal signs of pneumonitis or pneumonia on chest radiography. Chronic changes include those of bronchiectasis (bronchial wall thickening and dilatation).

Cardiomegaly and pulmonary oedema may be present on chest radiography.

Sweat test: sweat chloride 60 mmol/L or greater (60 mEq/L or greater) on repeat samples is diagnostic (levels of 40-59 mmol/L should be considered as indeterminate and suspicious). [49]

Ciliary studies (light and electron microscopy) reveal abnormal ciliary movement and structure.Situs inversus (dextrocardia and abnormally situated gastric bubble) may be present on standing chest x-ray.

Bronchoscopy demonstrating collapse of the trachea during expiration.

Bronchoscopy demonstrating collapse of the bronchus during expiration.

In bacterial bronchitis the sputum culture will most commonly isolate Haemophilus influenzae or Streptococcus pneumoniae. [51]

Exercise testing may reproduce the characteristic symptoms.Spirometry during an episode demonstrates blunting of inspiratory volume loop.

No obstructive pattern on spirometry during a hyperventilation episode.

Exercise testing may help distinguish.

Retinoscopy can easily distinguish between simple myopia, in which neutralisation of the reflex is obtained in all meridians by the same dioptric power, and astigmatism, where different dioptric powers are required in different meridians. [24]

Retinoscopy can easily distinguish between simple hyperopia, in which neutralisation of the reflex is obtained in all meridians by the same dioptric power, and astigmatism, where different dioptric powers are required in different meridians. [24]

Cataract can be easily diagnosed and graded using slit lamp biomicroscopy. The presence of cataract does not rule out co-existing astigmatism and therefore refraction also should be determined. [34]

Strabismus can be diagnosed by cover-uncover test, in which an occluder is used for alternate covering of the eyes in order to detect an obvious or a hidden eye deviation. The presence of strabismus does not rule out co-existing astigmatism, and therefore refraction should also be determined. [34]

The diagnosis can be achieved by a thorough fundus examination and confirmed by fluorescein angiography. [34]

MRI: typically, more localised lesions that may be multiple, and with proportionally more vasogenic oedema.Chest-abdominal CT scan, bone scan, and PET scan provide evidence of systemic disease.Histology provides a definitive diagnosis.

MRI demonstrates a thinner capsule toward the ventricle, with restricted diffusion of pus and elevated lactate level; may show multiple lesions.Blood tests suggestive of infection: for example, elevated WBC count, elevated erythrocyte sedimentation rate (ESR), and elevated C-reactive protein (CRP), with sensitivity 90% and specificity 77%. [31]Biopsy or aspiration provides the definite diagnosis, demonstrating pus (inflammatory cells), no tumour cells, and a positive culture of bacterial agent or fungus.

MRI shows multiple lesions in the periventricular white matter; may or may not enhance.CSF shows oligoclonal bands.Histology provides the definitive diagnosis, demonstrating demyelinating lesions, inflammatory cells, and absence of tumour cells, but usually is not necessary.

PET scan is cold.Histology provides definitive diagnosis (no tumour cells and extensive necrosis).

MRI shows typical vasculature distribution and restricted diffusion.

CSF shows leukocytosis, Herpes simplex virus (HSV) antibodies, and/or RBCs.EEG is characteristic with periodic lateralising epileptiform discharges.CT or MRI shows oedematous temporal lobes and haemorrhagic transformation.Brain biopsy is definitive with virus isolation.

CT scan demonstrates calcification in 90% of cases.Cortical location on MRI.Histology provides definitive diagnosis with classic fried egg cytoplasm and chicken wire vasculature.

MRI demonstrates a cortical lesion with distinct margins.CT may show deformity over the calvaria.Histopathology provides definitive diagnosis.

MRI commonly demonstrates medial temporal lobe lesion with cystic components and/or calcifications.Histology is definitive with characteristic cell types: ganglion and glial cells.

Clinical exam is the best tool to differentiate between these lesions.

Elimination of irritant will result in clinical improvement.Patch testing may be positive for relevant irritant.May be limited role for skin biopsy (e.g., patch tests are negative, chronic disease, uncertain diagnosis), which can identify whether contact dermatitis is present, but does not distinguish irritant from allergic contact dermatitis.

Elimination of allergic stimuli results in resolution of dermatitis.Patch testing may be positive for relevant allergen.May be limited role for skin biopsy (e.g., patch tests are negative, chronic disease, uncertain diagnosis), which can identify whether contact dermatitis is present, but does not distinguish irritant from allergic contact dermatitis.

Microscopy may reveal mites, eggs or scybala (mite faeces).

This is usually a clinical diagnosis. No laboratory testing is typically necessary to distinguish between atopic dermatitis and psoriasis. If the diagnosis is uncertain, there may be a limited role for skin biopsy which may not always reveal the classic features of psoriasis.

Skin biopsy is necessary to make the diagnosis of mycosis fungoides.

ECG shows uncoordinated atrial activation with rapidly oscillating, fibrillatory waves that vary in amplitude, shape, and timing. [7]

Generally, by ECG, atrial tachycardia has isoelectric intervals between the P waves in all leads. At very high atrial rates, it may be extremely difficult to distinguish the two. [7]

ECG will most frequently reveal left atrial hypertrophy. Echocardiogram will show stenosis of the mitral valve.

Echocardiogram will reveal the valvular vegetation. Blood culture indicates the causative organism.

Echocardiogram or MRI/CT scan will reveal the thrombus. Echocardiogram will also identify the catheter that is commonly associated with the formation of the thrombus. Rarely a transvenous biopsy may be indicated.

Specific ANAs in the blood may identify the disease process. ECG findings in connective tissue disease are non-specific with no differentiating features.

Imaging studies (e.g., CT scan and MRI) will reveal cardiac tumour.

Atrial septum intact with dilated right heart structures: identified by echocardiography in children, and MRI or CT in adults.

VSD identified by Doppler echocardiography.

PDA identified by Doppler echocardiography.

Pulmonary stenosis identified by Doppler echocardiography.

ECG shows right bundle-branch block.Echocardiography shows no evidence of an ASD.

Abnormal anatomy identified by Doppler echocardiography.

Comparison of numerous ECGs obtained at different times (i.e., days or months apart) may be useful. Baseline ECGs showing profound first-degree AV block may also help make the diagnosis.

Variations in the heart rate and the PR and RP (QRS to P) intervals suggest against the diagnosis of SVT. Comparison of numerous ECGs may be very useful.

Careful inspection of the ECG should allow distinction between these diagnoses.